Objective Exposure to microgravity results in postflight cardiovascular deconditioning in astronauts.Vascular oxidative stress injury and mitochondrial dysfunction have been reported during this process.To elucidate t...Objective Exposure to microgravity results in postflight cardiovascular deconditioning in astronauts.Vascular oxidative stress injury and mitochondrial dysfunction have been reported during this process.To elucidate the mechanism for this condition,we investigated whether mitochondrial oxidative stress regulates calcium homeostasis and vasoconstriction in hindlimb unweighted(HU)rat cerebral arteries.Methods Three-week HU was used to simulate microgravity in rats.The contractile responses to vasoconstrictors,mitochondrial fission/fusion,Ca^(2+) distribution,inositol 1,4,5-trisphosphate receptor(IP3 R)abundance,and the activities of voltage-gated K+channels(KV)and Ca^(2+)-activated K+channels(BKCa)were examined in rat cerebral vascular smooth muscle cells(VSMCs).Results An increase of cytoplasmic Ca^(2+) and a decrease of mitochondrial/sarcoplasmic reticulum(SR)Ca^(2+) were observed in HU rat cerebral VSMCs.The abundance of fusion proteins(mitofusin 1/2[MFN1/2])and fission proteins(dynamin-related protein 1[DRP1]and fission-mitochondrial 1[FIS1])was significantly downregulated and upregulated,respectively in HU rat cerebral VSMCs.The cerebrovascular contractile responses to vasoconstrictors were enhanced in HU rats compared to control rats,and IP3 R protein/mRNA levels were significantly upregulated.The current densities and open probabilities of KV and BKCa decreased and increased,respectively.Treatment with the mitochondrial-targeted antioxidant mitoTEMPO attenuated mitochondrial fission by upregulating MFN1/2 and downregulating DRP1/FIS1.It also decreased IP3 R expression levels and restored the activities of the KV and BKCa channels.MitoTEMPO restored the Ca^(2+) distribution in VSMCs and attenuated the enhanced vasoconstriction in HU rat cerebral arteries.Conclusion The present results suggest that mitochondrial oxidative stress enhances cerebral vasoconstriction by regulating calcium homeostasis during simulated microgravity.展开更多
OBJECTIVE To investigate the vasorelaxant effect of pinocembrin(5,7-dihydroxyflavanone),one of the main flavonoids in propolis,on angiotensinⅡ(AngⅡ)induced vasoconstriction and the molecular mechanism of action.METH...OBJECTIVE To investigate the vasorelaxant effect of pinocembrin(5,7-dihydroxyflavanone),one of the main flavonoids in propolis,on angiotensinⅡ(AngⅡ)induced vasoconstriction and the molecular mechanism of action.METHODS The isometric vascular tone was measured in thoracic aortic rings from SD rat,and the effects of pinocembrin on the single dose and concentration cumulative response curves of AngⅡ were recorded.The binding of pinocembrin to the angiotensin type 1 receptor(AT1R)was studied by using molecule docking analysis.Intracellular[Ca2+]([Ca2+]i)was measured with Fura2/AM in VSMCs.The phosphorylation levels of myosin light chain 2(MLC2)and myosin phosphatase target unit 1(MYPT1),and protein level of Rho kinase 1(ROCK1)in the rat aortic rings were detected by Western blotting.RESULTS Pinocembrin was observed to inhibit AngⅡ-induced vasoconstriction in rat aortic rings with either intact or denuded endothelium.In endothelium-denuded tissues,pinocembrin(pD′2 4.28±0.15)counteracted the contractions evoked by cumulative concentrations of AngⅡ.In a docking model,pinocembrin showed effective binding at the active site of AT1R.Pinocembrin was shown to inhibit both AngⅡ-induced Ca2+ release from internal stores and Ca2+ influx.Moreover,the increase in the phosphorylation of MLC2 and MYPT1,and the increased protein level of ROCK1 induced by AngⅡ was blocked by pinocembrin.CONCLUSION Pinocembrin inhibits AngⅡ-induced rat aortic ring contraction in a Ca2+-dependent and Ca2+-independent manner via blocking AT1R.展开更多
The present study attempted to test a novel hypothesis that Ca^2＋ sparks play an important role in arterial relaxation induced by tacrolimus. Recorded with confocal laser scanning microscopy, tacrolimus（10 μmol/L）...The present study attempted to test a novel hypothesis that Ca^2＋ sparks play an important role in arterial relaxation induced by tacrolimus. Recorded with confocal laser scanning microscopy, tacrolimus（10 μmol/L） increased the frequency of Ca^2＋ sparks, which could be reversed by ryanodine（10 μmol/L）. Electrophysiological experiments revealed that tacrolimus（10 μmol/L） increased the large-conductance Ca^2＋-activated K＋ currents（BKCa） in rat aortic vascular smooth muscle cells（AVSMCs）, which could be blocked by ryanodine（10 μmol/L）. Furthermore, tacrolimus（10 and 50 μmol/L） reduced the contractile force induced by norepinephrine（NE） or KCl in aortic vascular smooth muscle in a concentration-dependent manner, which could be also significantly attenuated by iberiotoxin（100 nmol/L） and ryanodine（10 μmol/L） respectively. In conclusion, tacrolimus could indirectly activate BKCa currents by increasing Ca^2＋ sparks released from ryanodine receptors, which inhibited the NE- or KCl-induced contraction in rat aorta.展开更多
Subarachnoid hemorrhage leads to a series of pathological changes,including vascular spasm,cellular apoptosis,blood–brain barrier damage,cerebral edema,and white matter injury.Microglia,which are the key immune cells...Subarachnoid hemorrhage leads to a series of pathological changes,including vascular spasm,cellular apoptosis,blood–brain barrier damage,cerebral edema,and white matter injury.Microglia,which are the key immune cells in the central nervous system,maintain homeostasis in the neural environment,support neurons,mediate apoptosis,participate in immune regulation,and have neuroprotective effects.Increasing evidence has shown that microglia play a pivotal role in the pathogenesis of subarachnoid hemorrhage and affect the process of injury and the prognosis of subarachnoid hemorrhage.Moreover,microglia play certain neuroprotective roles in the recovery phase of subarachnoid hemorrhage.Several approaches aimed at modulating microglia function are believed to attenuate subarachnoid hemorrhage injury.This provides new targets and ideas for the treatment of subarachnoid hemorrhage.However,an in-depth and comprehensive summary of the role of microglia after subarachnoid hemorrhage is still lacking.This review describes the activation of microglia after subarachnoid hemorrhage and their roles in the pathological processes of vasospasm,neuroinflammation,neuronal apoptosis,blood–brain barrier disruption,cerebral edema,and cerebral white matter lesions.It also discusses the neuroprotective roles of microglia during recovery from subarachnoid hemorrhage and therapeutic advances aimed at modulating microglial function after subarachnoid hemorrhage.Currently,microglia in subarachnoid hemorrhage are targeted with TLR inhibitors,nuclear factor-κB and STAT3 pathway inhibitors,glycine/tyrosine kinases,NLRP3 signaling pathway inhibitors,Gasdermin D inhibitors,vincristine receptorαreceptor agonists,ferroptosis inhibitors,genetic modification techniques,stem cell therapies,and traditional Chinese medicine.However,most of these are still being evaluated at the laboratory stage.More clinical studies and data on subarachnoid hemorrhage are required to improve the treatment of subarachnoid hemorrhage.展开更多
Introduction:Hypoxic pulmonary vasoconstriction(HPV)can be a challenging clinical problem.It is not fully elucidated where in the circulation the regulation of resistance takes place.It is often referred to as if it i...Introduction:Hypoxic pulmonary vasoconstriction(HPV)can be a challenging clinical problem.It is not fully elucidated where in the circulation the regulation of resistance takes place.It is often referred to as if it is in the arteries,but we hypothesized that it is in the venous side of the pulmonary circulation.Methods:In an open thorax model,pigs were treated with a veno-venous extra corporeal membrane oxygenator to either oxygenate or deoxygenate blood passing through the pulmonary vessels.At the same time the lungs were ventilated with extreme variations of inspired air from 5%to 100%oxygen,making it possible to make combinations of high and low oxygen content through the pulmonary circulation.A flow probe was inserted around the main pulmonary artery and catheters in the pulmonary artery and in the left atrium were used for pressure monitoring and blood tests.Under different combinations of oxygenation,pulmonary vascular resistance(PVR)was calculated.Results:With unchanged level of oxygen in the pulmonary artery and reduced inspired oxygen fraction lowering oxygen tension from 29 to 6.7 kPa in the pulmonary vein,PVR was doubled.With more extreme hypoxia PVR suddenly decreased.Combinations with low oxygenation in the pulmonary artery did not systematic influence PVR if there was enough oxygen in the inspired air and in the pulmonary veins.Discussion:The impact of hypoxia occurs from the alveolar level and forward with the blood flow.The experiments indicated that the regulation of PVR is mediated from the venous side.展开更多
One specific example reflecting the completity ofcardiovascular responses induced by serotonin(5-hydroxytryptamine;5-HT)and the progress achieved inthe pharmacological characterization of the receptorsinvolved can be ...One specific example reflecting the completity ofcardiovascular responses induced by serotonin(5-hydroxytryptamine;5-HT)and the progress achieved inthe pharmacological characterization of the receptorsinvolved can be illustrated by the effects of 5-HT on thecanine external carotid artery bed.Within thisframework,it has been shown that the external carotidvasoconstrictor response to 5-HT in the dog is mediatedby'5-HT_(1)-like'receptors,which being blocked by the5-HT_(1B/1D)receptor antagonist GR127935,resemble 5-HT_(1B/1D)(previously called 5-HT_(1B/1D))receptors.It was proposed that these receptors coilld belong to the 5-HT_(lB),rather than the 5-HT_(lD),subtype on the basis of their resistance to blockade by a high dose of ritanserin(a potential 5-HT_(lD)receptor antagomst and the presence of mRNA for 5-HT_(lB)(5-HT_(lDB))receptors,but not for 5-HT_(lD)(5-HT_(lD))receptors,in vascalar smooth muscle.With the advent of subtype-selective antagonists it was subsequently shown that the external carotid vasocenstriction to 5-HT and surmantriptan is dose-dependently antagonized by the selective 5-HT_(lB)receptor antagonist SB224289[2,3,6.7-telrahydro-I'-methyl-5-[2'-methyl-4(5-methyl-1,2,4-oxadiazol-3-y1)biphenyl-4-carbonyl]]furo[2,3-f]indole-3-spiro-4'-piperidine hydrochloride],whereas the selective 5-HT_(lD)receptor antagonist BRL15572[l(3-chloropheny1)-4-[3,3-diphenyl(2-(S,R)hydroxypropany1)piperazine]hydrochloride was inefective.These findings represent the first in vivo evidence showing that vascular constriction induced by 5-HT and sumatriptan is mediated primarily via 5-HT_(lB),but not 5-HT_(lD)receptors.The pharmacological profile of these receptors could be similar(isolated human temporal artery and porcine carotid arteriovenous anastomoses)to other putative 5-HT_(lB)receptors mediating vasoconstrictor responses.In view of the putative pathophysiologic role of external carotid(and extracerebral)vasodilation in migraine,the constriction of these blood vessels by sumatriptan via 5-HT_(lB)receptors may be,at least partly,responsible for its therapeutic efficacy in migraine.展开更多
Background: Primary intraventricular hemorrhage is an uncommon cause of stroke and is often associated with longstanding, uncontrolled hypertension. Reversible cerebral vasoconstriction is also an uncommon condition c...Background: Primary intraventricular hemorrhage is an uncommon cause of stroke and is often associated with longstanding, uncontrolled hypertension. Reversible cerebral vasoconstriction is also an uncommon condition characterized by reversible constriction of intracerebral vessels, which can lead to ischemic or hemorrhagic strokes. Case presentation: We describe a case of isolated primary intraventricular hemorrhage secondary to reversible cerebral vasoconstriction syndrome triggered by pseudoephedrine. Conclusions: Reversible cerebral vasoconstriction syndrome is a rare cause of primary intraventricular hemorrhage and should be considered in the differential in angiography-negative IVH when there is a history of vasoactive substance use.展开更多
Normal tension glaucoma(NTG)is a multifactorial optic neuropathy characterized by normal intraocular pressure,progressive retinal ganglion cell(RGC)death,and glaucomatous visual field loss.Recent studies have describe...Normal tension glaucoma(NTG)is a multifactorial optic neuropathy characterized by normal intraocular pressure,progressive retinal ganglion cell(RGC)death,and glaucomatous visual field loss.Recent studies have described the mechanisms underlying the pathogenesis of NTG.In addition to controlling intraocular pressure,neuroprotection and reduction of RGC degeneration may be beneficial therapies for NTG.In this review,we summarized the main regulatory mechanisms of RGC death in NTG,including autophagy,glutamate neurotoxicity,oxidative stress,neuroinflammation,immunity,and vasoconstriction.Autophagy can be induced by retinal hypoxia and axonal damage.In this process,ischemia can cause mutations of optineurin and activate the nuclear factor-kappa B pathway.Glutamate neurotoxicity is induced by the over-stimulation of N-methyl-D-aspartate membrane receptors by glutamate,which occurs in RGCs and induces progressive glaucomatous optic neuropathy.Oxidative stress also participates in NTG-related glaucomatous optic neuropathy.It impairs the mitochondrial and DNA function of RGCs through the apoptosis signal-regulating kinase-JUN N-terminal kinase pathway.Moreover,it increases inflammation and the immune response of RGCs.Endothelin 1 causes endothelial dysfunction and impairment of ocular blood flow,promoting vasospasm and glaucomatous optic neuropathy,as a result of NTG.In conclusion,we discussed research progress on potential options for the protection of RGCs,including TANK binding kinase 1 inhibitors regulating autophagy,N-methyl-D-aspartate receptor antagonists inhibiting glutamate toxicity,ASK1 inhibitors regulating mitochondrial function,and antioxidants inhibiting oxidative stress.In NTG,RGC death is regulated by a network of mechanisms,while various potential targets protect RGCs.Collectively,these findings provide insight into the pathogenesis of NTG and potential therapeutic strategies.展开更多
BACKGROUND There are two known types of exercise-induced acute renal failure.One is the long-known myoglobinuria-induced acute renal failure due to severe rhabdomyolysis,and the other is the recently recognized non-my...BACKGROUND There are two known types of exercise-induced acute renal failure.One is the long-known myoglobinuria-induced acute renal failure due to severe rhabdomyolysis,and the other is the recently recognized non-myoglobinuria-induced acute renal failure with mild rhabdomyolysis.Exercise-induced acute renal failure was first reported in 1982.Non-myoglobinuria-induced acute renal failure is associated with severe low back pain and patchy renal vasoconstriction,and it is termed post-exercise acute renal failure because it usually occurs hours after exercise.It is also called acute renal failure with severe loin pain and patchy renal ischemia after anaerobic exercise(ALPE).AIM To makes a significant contribution to medical literature as it presents a study that investigated a not-widely-known type of exercise-induced acute renal failure known as ALPE.METHODS We performed a database search selecting papers published in the English or Japanese language.A database search was lastly accessed on September 1,2022.The results of this study were compared with those reported in other case series.RESULTS The study evaluated renal hypouricemia as a key risk factor of ALPE.The development of ALPE is due to the sum of risk factors such as exercise,hypouricemia,nonsteroidal anti-inflammatory drugs,vasopressors,and dehydration.CONCLUSION In conclusion,hypouricemia plays a key role in the development of ALPE and is often associated with anaerobic exercise.The development of ALPE is a result of the cumulative effects of risk factors such as exercise,hypouricemia,NSAIDs,vasopressors,and dehydration.展开更多
In vertebrates, non-lens βγ-crystallins are widely expressed in various tissues and their functions are not well known. The molecular mechanisms of trefoil factors （TFFs）, which involved in mucosal healing and tum...In vertebrates, non-lens βγ-crystallins are widely expressed in various tissues and their functions are not well known. The molecular mechanisms of trefoil factors （TFFs）, which involved in mucosal healing and tumorigenesis, have remained elusive. βγ-CAT is a novel multifunctional protein complex of non-lens βγ-crystallin and trefoil factor from frog skin secretions. Here we report that βγ-CAT could induce sustained contraction of isolated rabbit aortic rings in dosage （2-35nmol/L） and endothelium dependent manners （P〈0.01 ）. In addition, in situ immunofluorescence indicated that positive TNF-α signals were mainly detected at the endothelial cell layer of βγ-CAT （25nmol/L） treated rings. Furthermore, βγ-CAT induced primary cultured rabbit thoracic aortic endothelial cells （RAECs） rapidly to release TNF-α. After βγ-CAT （25nmol/L） treated for 10 and 30min, the levels of the endothelial cells released TNF-ct were 34.17±5.10 pg/mL and 98.01±4.67 pg/mL （P〈0.01）, respectively. In conclusion, βγ-CAT could induce sustained contraction of isolated aortic rings, and the contractile effect might be partially explained by the release of TNF-α. These findings will give new insight into understanding the functions and physiological roles of non-lens βγ-crystallins and trefoil factors.展开更多
Hypoxic pulmonary hypertension (HPH) is a common complication in patients with chronic obstructive pulmonary disease (COPD), sleep-disordered breathing, or dwellers in high altitude. The exact mechanisms underlying th...Hypoxic pulmonary hypertension (HPH) is a common complication in patients with chronic obstructive pulmonary disease (COPD), sleep-disordered breathing, or dwellers in high altitude. The exact mechanisms underlying the development of HPH still remain unclear. Reactive oxygen species (ROS),hypoxia inducible factors (HIF), and potassium channels (KV) are believed as the main factors during the development of HPH. We propose that the “ROS/Kv/HIF axis” may play an important initiating role in the development of HPH. Being formed under a hypoxic condition, ROS affects the expression and function of HIFs or KV, and consequently triggers multiple downstream signaling pathways and genes expression that participate in promoting pulmonary vasoconstriction and arterial remodeling. Thus, further study determining the initiating role of “ROS/Kv/HIF axis” in the development of HPH could provide theoretic evidences to better understand the underlying mechanisms of HPH, and help identify new potential targets in the treatment of HPH.展开更多
Characteristic findings in patients with cirrhosis are vasodilatation with low overall systemic vascular resistance, high arterial compliance, increased cardiac output, secondary activation of counter-regulatory syste...Characteristic findings in patients with cirrhosis are vasodilatation with low overall systemic vascular resistance, high arterial compliance, increased cardiac output, secondary activation of counter-regulatory systems （renin-angiotensin-aldosterone system, sympathetic nervous system, release of vasopressin）, and resistance to vasopressors. The vasodilatory state is mediated through adrenomedullin, calcitonin generelated peptide, nitric oxide, and other vasodilators, and is most pronounced in the splanchnic area. This constitutes an effective （although relative） counterbalance to increased arterial blood pressure. This review considers the alterations in systemic hemodynamics in patients with cirrhosis in relation to essential hypertension and arterial hypertension of the renal origin. Subjects with arterial hypertension （essential, secondary） may become normotensive during the development of cirrhosis, and arterial hypertension is rarely manifested in patients with cirrhosis, even in cases with renovascular disease and high circulating renin activity. There is much dispute as to the understanding of homoeostatic regulation in cirrhotic patients with manifest arterial hypertension. This most likely includes the combination of vasodilatation and vasoconstriction in parallel.展开更多
Acute brain injury caused by subarachnoid hemorrhage is the major cause of poor prognosis. The pathology of subarachnoid hemorrhage likely involves major morphological changes in the microcirculation. However, previou...Acute brain injury caused by subarachnoid hemorrhage is the major cause of poor prognosis. The pathology of subarachnoid hemorrhage likely involves major morphological changes in the microcirculation. However, previous studies primarily used fixed tissue or delayed injury models. Therefore, in the present study, we used in vivo imaging to observe the dynamic changes in cerebral microcirculation after subarachnoid hemorrhage. Subarachnoid hemorrhage was induced by perforation of the bifurcation of the middle cerebral and anterior cerebral arteries in male C57/BL6 mice. The diameter of pial arterioles and venules was measured by in vivo fluorescence microscopy at different time points within 180 minutes after subarachnoid hemorrhage. Cerebral blood flow was examined and leukocyte adhesion/albumin extravasation was determined at different time points before and after subarachnoid hemorrhage. Cerebral pial microcirculation was abnormal and cerebral blood flow was reduced after subarachnoid hemorrhage. Acute vasoconstriction occurred predominantly in the arterioles instead of the venules. A progressive increase in the number of adherent leukocytes in venules and substantial albumin extravasation were observed between 10 and 180 minutes after subarachnoid hemorrhage. These results show that major changes in microcirculation occur in the early stage of subarachnoid hemorrhage. Our findings may promote the development of novel therapeutic strategies for the early treatment of subarachnoid hemorrhage.展开更多
The influence of hypoxia on the activity of voltage-gated potassium channel in pulmonary artery smooth muscle cells （PASMCs） of rats and its roles in the pathogenesis of chronic pulmonary heart disease were investig...The influence of hypoxia on the activity of voltage-gated potassium channel in pulmonary artery smooth muscle cells （PASMCs） of rats and its roles in the pathogenesis of chronic pulmonary heart disease were investigated. Eighty male Sprague-Dawley rats were randomly allocated into control group （n=10）, acute hypoxic group （n=10）, and chronic hypoxic groups （n=60）. The chronic hypoxic groups were randomly divided into 6 subgroups （n=10 each） according to the chronic hypoxic periods. The rats in the control group were kept in room air and those in acute hypoxic group in hypoxia envi- ronmental chamber for 8 h. The rats in chronic hypoxic subgroups were kept in hypoxia environmental chamber for 8 h per day for 5, 10, 15, 20, 25, and 30 days, respectively. The mean pulmonary arterial pressure （mPAP）, right ventricular hypertrophy index （RVHI）, and the current of voltage-gated potas- sium channel （IK） in PASMCs were measured. Results showed that both acute and chronic hypoxia could decrease the IK in PASMCs of rats and the I-V relationship downward shifted to the right. And the peak Ir density at ＋60mV decreased with prolongation of hypoxia exposure. No significant difference was noted in the density oflK （at ＋60 mV） and I-V relationship between control group and chronic hy- poxic subgroup exposed to hypoxia for 5 days （P〉0.05）, but there was a significant difference between control group and chronic hypoxic subgroup exposed to hypoxia for 10 days （P〈0.05）. Significant dif- ferences were noted in the IK density （at ＋60 mV） and I-V relationships between control group and chronic hypoxic subgroups exposed to hypoxia for 20 days and 30 days （P〈0.01）. Compared with con- trol rats, the mPAP and RVHI were significantly increased after chronic exposure to hypoxia for 10 days （P〈0.05）, which were further increased with prolongation of hypoxia exposure, and there were signifi- cant differences between control group and chronic hypoxic subgroups exposed to hypoxia for 20 days and 30 days （P〈0.01）. Both the mPAP and the RVHI were negatively correlated with the density OflK （r---0.89769 and -0.94476, respectively, both P〈0.01）. It is concluded that exposure to hypoxia may cause decreased activity of voltage-gated potassium channel, leading to hypoxia pulmonary vasocon- striction （HPV）. Sustained HPV may result in chronic pulmonary hypertension, even chronic pulmonary heart disease, contributing to the pathogenesis of chronic pulmonary heart disease.展开更多
Literature concerning procoagulant activity of the amniotic fluid and pathomechanism of amniotic fluid embolism (AFE) was surveyed and a new concept of its pathogenesis, called the integrated concept of AFE, was prese...Literature concerning procoagulant activity of the amniotic fluid and pathomechanism of amniotic fluid embolism (AFE) was surveyed and a new concept of its pathogenesis, called the integrated concept of AFE, was presented. According to this concept, two components of the amniotic fluid are involved: (i) apoptosis-affected amniotic cells showing a special role in the initiation of disseminated intravascular coagulation (DIC) and (ii) leukotrienes (formerly called slow-reacting substances), inducing bronchial and pulmonary vascular smooth muscle contraction. Although each of these components initiates a different pathogenic pathway, they both lead to the formation of a mechanical barrier on blood flow through the lungs (amniotic debris + microemboli) and/or functional barrier (pulmonary vasoconstriction). An old dilemma, concerning indications for heparin therapy in AFE was recalled in the light of the new concept.展开更多
AIM:To study the effect of circulating cell-free oxy-hemoglobin(FHb) on intestinal microcirculation and intestinal epithelial injury in a rat model. METHODS:To induce elevated intravascular circulating FHb,male Spragu...AIM:To study the effect of circulating cell-free oxy-hemoglobin(FHb) on intestinal microcirculation and intestinal epithelial injury in a rat model. METHODS:To induce elevated intravascular circulating FHb,male Sprague-Dawley rats received water or FHb infusion.Microcirculatory changes in jejunum,ileum and colon were evaluated using fluorescent microspheres.Intestinal injury was quantified as plasmatic release of ileal lipid binding protein(iLBP) and verified by histological analysis of the ileum. RESULTS:Water and FHb infusions resulted,when compared with saline infusion,in reduced intestinal microcirculation(after 30 min P<0.05,or better;after 60 min FHb infusion P<0.05 for jejunum and colon) .Circulating FHb levels correlated significantly with release of iLBP(Spearman r=0.72,P=0.0011) .Epithelial cell injury of the villi was histologically observed after water and FHb infusions. CONCLUSION:This study shows that circulating FHb leads to a reduction in intestinal microcirculatory blood flow with marked injury to intestinal epithelial cells. These data support the hypothesis that circulating FHb contributes to the development of intestinal injury.展开更多
The objective of this report is to describe the possible use of intramiometrial vasoconstrictive agents for laparoscopic management of interstitial pregnancy and the consequences in anatomical results and reproductive...The objective of this report is to describe the possible use of intramiometrial vasoconstrictive agents for laparoscopic management of interstitial pregnancy and the consequences in anatomical results and reproductive outcomes. Cornual resection can be performed by laparoscopy, but the high vascularization of this area may result in profuse bleeding and laparoscopic suturing under these conditions might be impossible for the majority of the surgeons. We present a case that describes the possible use of intramiometrial instillation of a solution of diluted epinephrine and levobupivacaine under laparoscopic guidance that permitted a bloodless cornual excision with complete reconstruction. Vasoactive agents might have potentially serious cardiovascular side effects and the correct election of the active principle and the dosage is essential to reduce the risk of the surgery and obtain good anatomical results and reproductive outcomes. In conclusion, unruptured interstitial pregnancies can be managed successfully with intramyometrial instillation of epinephrine and bupivacaine. This simple technique is particularly attractive as it facilitates anatomical reconstruction of the cornual area, gives enough time to perform a complete suture of the defect and reduces the risk of laparotomic conversion.展开更多
Objecive To observe the eventual thermic effects of stimulaing Tàixī (太溪 KI 3) by telethermography. Methods Nine individuals of both sexes, chosen randomly, paricipated in this study. The temperature of the ro...Objecive To observe the eventual thermic effects of stimulaing Tàixī (太溪 KI 3) by telethermography. Methods Nine individuals of both sexes, chosen randomly, paricipated in this study. The temperature of the room where the experiment was carried out was not above 21 ℃. At the start of the experiment the volunteer stayed for exactly ten minutes in the room for acclimaizaion, then the first thermographic image was recorded for standardizaion purposes. Following this, an acupuncture needle was inserted at KI 3 only in the right leg, whose depth was limited to obtain Deqi, only manual stimulation for 15 min permanence in the site. Ater this period, new images were recorded. Results Significant reduction of all the right leg temperatures, by about 1.1 ℃ in all the volunteers that received the acupuncture at the Kl 3 was noted, with a coefficient variaion of P<0.0001 that was staisically highly significant, while on the other not simulated leg the variaion that occurred was around 0.7 ℃, with no significant coefficient variation of P>0.05. Conclusion The results of this study demonstrate that manual simulaion of the Kl 3 influences significantly peripheral vascular circulation, by means of sympathetic stimulaion causing vasoconstricion.展开更多
基金supported by the National Natural Science Foundation of China[81871516,81571841]Youth Special Project of Chinese PLA General Hospital[QNC19052]。
文摘Objective Exposure to microgravity results in postflight cardiovascular deconditioning in astronauts.Vascular oxidative stress injury and mitochondrial dysfunction have been reported during this process.To elucidate the mechanism for this condition,we investigated whether mitochondrial oxidative stress regulates calcium homeostasis and vasoconstriction in hindlimb unweighted(HU)rat cerebral arteries.Methods Three-week HU was used to simulate microgravity in rats.The contractile responses to vasoconstrictors,mitochondrial fission/fusion,Ca^(2+) distribution,inositol 1,4,5-trisphosphate receptor(IP3 R)abundance,and the activities of voltage-gated K+channels(KV)and Ca^(2+)-activated K+channels(BKCa)were examined in rat cerebral vascular smooth muscle cells(VSMCs).Results An increase of cytoplasmic Ca^(2+) and a decrease of mitochondrial/sarcoplasmic reticulum(SR)Ca^(2+) were observed in HU rat cerebral VSMCs.The abundance of fusion proteins(mitofusin 1/2[MFN1/2])and fission proteins(dynamin-related protein 1[DRP1]and fission-mitochondrial 1[FIS1])was significantly downregulated and upregulated,respectively in HU rat cerebral VSMCs.The cerebrovascular contractile responses to vasoconstrictors were enhanced in HU rats compared to control rats,and IP3 R protein/mRNA levels were significantly upregulated.The current densities and open probabilities of KV and BKCa decreased and increased,respectively.Treatment with the mitochondrial-targeted antioxidant mitoTEMPO attenuated mitochondrial fission by upregulating MFN1/2 and downregulating DRP1/FIS1.It also decreased IP3 R expression levels and restored the activities of the KV and BKCa channels.MitoTEMPO restored the Ca^(2+) distribution in VSMCs and attenuated the enhanced vasoconstriction in HU rat cerebral arteries.Conclusion The present results suggest that mitochondrial oxidative stress enhances cerebral vasoconstriction by regulating calcium homeostasis during simulated microgravity.
基金The project supported by National Natural Science Foundation of China(81102444)the Major Scientific and Technological Special Project for"Significant New Drugs Creation"(2009ZX09302-003,2013ZX09508104)the Central Public Scientific Research Institution Fundamental Project(2014CX05)
文摘OBJECTIVE To investigate the vasorelaxant effect of pinocembrin(5,7-dihydroxyflavanone),one of the main flavonoids in propolis,on angiotensinⅡ(AngⅡ)induced vasoconstriction and the molecular mechanism of action.METHODS The isometric vascular tone was measured in thoracic aortic rings from SD rat,and the effects of pinocembrin on the single dose and concentration cumulative response curves of AngⅡ were recorded.The binding of pinocembrin to the angiotensin type 1 receptor(AT1R)was studied by using molecule docking analysis.Intracellular[Ca2+]([Ca2+]i)was measured with Fura2/AM in VSMCs.The phosphorylation levels of myosin light chain 2(MLC2)and myosin phosphatase target unit 1(MYPT1),and protein level of Rho kinase 1(ROCK1)in the rat aortic rings were detected by Western blotting.RESULTS Pinocembrin was observed to inhibit AngⅡ-induced vasoconstriction in rat aortic rings with either intact or denuded endothelium.In endothelium-denuded tissues,pinocembrin(pD′2 4.28±0.15)counteracted the contractions evoked by cumulative concentrations of AngⅡ.In a docking model,pinocembrin showed effective binding at the active site of AT1R.Pinocembrin was shown to inhibit both AngⅡ-induced Ca2+ release from internal stores and Ca2+ influx.Moreover,the increase in the phosphorylation of MLC2 and MYPT1,and the increased protein level of ROCK1 induced by AngⅡ was blocked by pinocembrin.CONCLUSION Pinocembrin inhibits AngⅡ-induced rat aortic ring contraction in a Ca2+-dependent and Ca2+-independent manner via blocking AT1R.
基金supported by the National Natural Science Foundation of China(No.81102439)
文摘The present study attempted to test a novel hypothesis that Ca^2＋ sparks play an important role in arterial relaxation induced by tacrolimus. Recorded with confocal laser scanning microscopy, tacrolimus（10 μmol/L） increased the frequency of Ca^2＋ sparks, which could be reversed by ryanodine（10 μmol/L）. Electrophysiological experiments revealed that tacrolimus（10 μmol/L） increased the large-conductance Ca^2＋-activated K＋ currents（BKCa） in rat aortic vascular smooth muscle cells（AVSMCs）, which could be blocked by ryanodine（10 μmol/L）. Furthermore, tacrolimus（10 and 50 μmol/L） reduced the contractile force induced by norepinephrine（NE） or KCl in aortic vascular smooth muscle in a concentration-dependent manner, which could be also significantly attenuated by iberiotoxin（100 nmol/L） and ryanodine（10 μmol/L） respectively. In conclusion, tacrolimus could indirectly activate BKCa currents by increasing Ca^2＋ sparks released from ryanodine receptors, which inhibited the NE- or KCl-induced contraction in rat aorta.
基金supported by the Natural Science Foundation of Shandong Province,No.ZR2022MH124the Youth Science Foundation of Shandong First Medical University,No.202201–105(both to YX)。
文摘Subarachnoid hemorrhage leads to a series of pathological changes,including vascular spasm,cellular apoptosis,blood–brain barrier damage,cerebral edema,and white matter injury.Microglia,which are the key immune cells in the central nervous system,maintain homeostasis in the neural environment,support neurons,mediate apoptosis,participate in immune regulation,and have neuroprotective effects.Increasing evidence has shown that microglia play a pivotal role in the pathogenesis of subarachnoid hemorrhage and affect the process of injury and the prognosis of subarachnoid hemorrhage.Moreover,microglia play certain neuroprotective roles in the recovery phase of subarachnoid hemorrhage.Several approaches aimed at modulating microglia function are believed to attenuate subarachnoid hemorrhage injury.This provides new targets and ideas for the treatment of subarachnoid hemorrhage.However,an in-depth and comprehensive summary of the role of microglia after subarachnoid hemorrhage is still lacking.This review describes the activation of microglia after subarachnoid hemorrhage and their roles in the pathological processes of vasospasm,neuroinflammation,neuronal apoptosis,blood–brain barrier disruption,cerebral edema,and cerebral white matter lesions.It also discusses the neuroprotective roles of microglia during recovery from subarachnoid hemorrhage and therapeutic advances aimed at modulating microglial function after subarachnoid hemorrhage.Currently,microglia in subarachnoid hemorrhage are targeted with TLR inhibitors,nuclear factor-κB and STAT3 pathway inhibitors,glycine/tyrosine kinases,NLRP3 signaling pathway inhibitors,Gasdermin D inhibitors,vincristine receptorαreceptor agonists,ferroptosis inhibitors,genetic modification techniques,stem cell therapies,and traditional Chinese medicine.However,most of these are still being evaluated at the laboratory stage.More clinical studies and data on subarachnoid hemorrhage are required to improve the treatment of subarachnoid hemorrhage.
文摘Introduction:Hypoxic pulmonary vasoconstriction(HPV)can be a challenging clinical problem.It is not fully elucidated where in the circulation the regulation of resistance takes place.It is often referred to as if it is in the arteries,but we hypothesized that it is in the venous side of the pulmonary circulation.Methods:In an open thorax model,pigs were treated with a veno-venous extra corporeal membrane oxygenator to either oxygenate or deoxygenate blood passing through the pulmonary vessels.At the same time the lungs were ventilated with extreme variations of inspired air from 5%to 100%oxygen,making it possible to make combinations of high and low oxygen content through the pulmonary circulation.A flow probe was inserted around the main pulmonary artery and catheters in the pulmonary artery and in the left atrium were used for pressure monitoring and blood tests.Under different combinations of oxygenation,pulmonary vascular resistance(PVR)was calculated.Results:With unchanged level of oxygen in the pulmonary artery and reduced inspired oxygen fraction lowering oxygen tension from 29 to 6.7 kPa in the pulmonary vein,PVR was doubled.With more extreme hypoxia PVR suddenly decreased.Combinations with low oxygenation in the pulmonary artery did not systematic influence PVR if there was enough oxygen in the inspired air and in the pulmonary veins.Discussion:The impact of hypoxia occurs from the alveolar level and forward with the blood flow.The experiments indicated that the regulation of PVR is mediated from the venous side.
基金Project supported by Consejo Nacional de Ciencia y Tecnologia(Mexico City)
文摘One specific example reflecting the completity ofcardiovascular responses induced by serotonin(5-hydroxytryptamine;5-HT)and the progress achieved inthe pharmacological characterization of the receptorsinvolved can be illustrated by the effects of 5-HT on thecanine external carotid artery bed.Within thisframework,it has been shown that the external carotidvasoconstrictor response to 5-HT in the dog is mediatedby'5-HT_(1)-like'receptors,which being blocked by the5-HT_(1B/1D)receptor antagonist GR127935,resemble 5-HT_(1B/1D)(previously called 5-HT_(1B/1D))receptors.It was proposed that these receptors coilld belong to the 5-HT_(lB),rather than the 5-HT_(lD),subtype on the basis of their resistance to blockade by a high dose of ritanserin(a potential 5-HT_(lD)receptor antagomst and the presence of mRNA for 5-HT_(lB)(5-HT_(lDB))receptors,but not for 5-HT_(lD)(5-HT_(lD))receptors,in vascalar smooth muscle.With the advent of subtype-selective antagonists it was subsequently shown that the external carotid vasocenstriction to 5-HT and surmantriptan is dose-dependently antagonized by the selective 5-HT_(lB)receptor antagonist SB224289[2,3,6.7-telrahydro-I'-methyl-5-[2'-methyl-4(5-methyl-1,2,4-oxadiazol-3-y1)biphenyl-4-carbonyl]]furo[2,3-f]indole-3-spiro-4'-piperidine hydrochloride],whereas the selective 5-HT_(lD)receptor antagonist BRL15572[l(3-chloropheny1)-4-[3,3-diphenyl(2-(S,R)hydroxypropany1)piperazine]hydrochloride was inefective.These findings represent the first in vivo evidence showing that vascular constriction induced by 5-HT and sumatriptan is mediated primarily via 5-HT_(lB),but not 5-HT_(lD)receptors.The pharmacological profile of these receptors could be similar(isolated human temporal artery and porcine carotid arteriovenous anastomoses)to other putative 5-HT_(lB)receptors mediating vasoconstrictor responses.In view of the putative pathophysiologic role of external carotid(and extracerebral)vasodilation in migraine,the constriction of these blood vessels by sumatriptan via 5-HT_(lB)receptors may be,at least partly,responsible for its therapeutic efficacy in migraine.
文摘Background: Primary intraventricular hemorrhage is an uncommon cause of stroke and is often associated with longstanding, uncontrolled hypertension. Reversible cerebral vasoconstriction is also an uncommon condition characterized by reversible constriction of intracerebral vessels, which can lead to ischemic or hemorrhagic strokes. Case presentation: We describe a case of isolated primary intraventricular hemorrhage secondary to reversible cerebral vasoconstriction syndrome triggered by pseudoephedrine. Conclusions: Reversible cerebral vasoconstriction syndrome is a rare cause of primary intraventricular hemorrhage and should be considered in the differential in angiography-negative IVH when there is a history of vasoactive substance use.
基金supported in part by the Technology Foundation of Tianjin Eye Hospital of China, No. YKQN1911 (to WCS)Tianjin Health Science and Technology Project, No. TJWJ2021QN071 (to WCS)Translational Medicine Research Project of State Key Laboratory of Experimental Hematology of China, No. Z21-11 (to BQH)
文摘Normal tension glaucoma(NTG)is a multifactorial optic neuropathy characterized by normal intraocular pressure,progressive retinal ganglion cell(RGC)death,and glaucomatous visual field loss.Recent studies have described the mechanisms underlying the pathogenesis of NTG.In addition to controlling intraocular pressure,neuroprotection and reduction of RGC degeneration may be beneficial therapies for NTG.In this review,we summarized the main regulatory mechanisms of RGC death in NTG,including autophagy,glutamate neurotoxicity,oxidative stress,neuroinflammation,immunity,and vasoconstriction.Autophagy can be induced by retinal hypoxia and axonal damage.In this process,ischemia can cause mutations of optineurin and activate the nuclear factor-kappa B pathway.Glutamate neurotoxicity is induced by the over-stimulation of N-methyl-D-aspartate membrane receptors by glutamate,which occurs in RGCs and induces progressive glaucomatous optic neuropathy.Oxidative stress also participates in NTG-related glaucomatous optic neuropathy.It impairs the mitochondrial and DNA function of RGCs through the apoptosis signal-regulating kinase-JUN N-terminal kinase pathway.Moreover,it increases inflammation and the immune response of RGCs.Endothelin 1 causes endothelial dysfunction and impairment of ocular blood flow,promoting vasospasm and glaucomatous optic neuropathy,as a result of NTG.In conclusion,we discussed research progress on potential options for the protection of RGCs,including TANK binding kinase 1 inhibitors regulating autophagy,N-methyl-D-aspartate receptor antagonists inhibiting glutamate toxicity,ASK1 inhibitors regulating mitochondrial function,and antioxidants inhibiting oxidative stress.In NTG,RGC death is regulated by a network of mechanisms,while various potential targets protect RGCs.Collectively,these findings provide insight into the pathogenesis of NTG and potential therapeutic strategies.
文摘BACKGROUND There are two known types of exercise-induced acute renal failure.One is the long-known myoglobinuria-induced acute renal failure due to severe rhabdomyolysis,and the other is the recently recognized non-myoglobinuria-induced acute renal failure with mild rhabdomyolysis.Exercise-induced acute renal failure was first reported in 1982.Non-myoglobinuria-induced acute renal failure is associated with severe low back pain and patchy renal vasoconstriction,and it is termed post-exercise acute renal failure because it usually occurs hours after exercise.It is also called acute renal failure with severe loin pain and patchy renal ischemia after anaerobic exercise(ALPE).AIM To makes a significant contribution to medical literature as it presents a study that investigated a not-widely-known type of exercise-induced acute renal failure known as ALPE.METHODS We performed a database search selecting papers published in the English or Japanese language.A database search was lastly accessed on September 1,2022.The results of this study were compared with those reported in other case series.RESULTS The study evaluated renal hypouricemia as a key risk factor of ALPE.The development of ALPE is due to the sum of risk factors such as exercise,hypouricemia,nonsteroidal anti-inflammatory drugs,vasopressors,and dehydration.CONCLUSION In conclusion,hypouricemia plays a key role in the development of ALPE and is often associated with anaerobic exercise.The development of ALPE is a result of the cumulative effects of risk factors such as exercise,hypouricemia,NSAIDs,vasopressors,and dehydration.
基金National Natural Science Foundation (30630014, 30570359)The grant of "Key Research Direction-KSCX2-YW-R-088" from Chinese Academy of Sciences~~
文摘In vertebrates, non-lens βγ-crystallins are widely expressed in various tissues and their functions are not well known. The molecular mechanisms of trefoil factors （TFFs）, which involved in mucosal healing and tumorigenesis, have remained elusive. βγ-CAT is a novel multifunctional protein complex of non-lens βγ-crystallin and trefoil factor from frog skin secretions. Here we report that βγ-CAT could induce sustained contraction of isolated rabbit aortic rings in dosage （2-35nmol/L） and endothelium dependent manners （P〈0.01 ）. In addition, in situ immunofluorescence indicated that positive TNF-α signals were mainly detected at the endothelial cell layer of βγ-CAT （25nmol/L） treated rings. Furthermore, βγ-CAT induced primary cultured rabbit thoracic aortic endothelial cells （RAECs） rapidly to release TNF-α. After βγ-CAT （25nmol/L） treated for 10 and 30min, the levels of the endothelial cells released TNF-ct were 34.17±5.10 pg/mL and 98.01±4.67 pg/mL （P〈0.01）, respectively. In conclusion, βγ-CAT could induce sustained contraction of isolated aortic rings, and the contractile effect might be partially explained by the release of TNF-α. These findings will give new insight into understanding the functions and physiological roles of non-lens βγ-crystallins and trefoil factors.
文摘Hypoxic pulmonary hypertension (HPH) is a common complication in patients with chronic obstructive pulmonary disease (COPD), sleep-disordered breathing, or dwellers in high altitude. The exact mechanisms underlying the development of HPH still remain unclear. Reactive oxygen species (ROS),hypoxia inducible factors (HIF), and potassium channels (KV) are believed as the main factors during the development of HPH. We propose that the “ROS/Kv/HIF axis” may play an important initiating role in the development of HPH. Being formed under a hypoxic condition, ROS affects the expression and function of HIFs or KV, and consequently triggers multiple downstream signaling pathways and genes expression that participate in promoting pulmonary vasoconstriction and arterial remodeling. Thus, further study determining the initiating role of “ROS/Kv/HIF axis” in the development of HPH could provide theoretic evidences to better understand the underlying mechanisms of HPH, and help identify new potential targets in the treatment of HPH.
文摘Characteristic findings in patients with cirrhosis are vasodilatation with low overall systemic vascular resistance, high arterial compliance, increased cardiac output, secondary activation of counter-regulatory systems （renin-angiotensin-aldosterone system, sympathetic nervous system, release of vasopressin）, and resistance to vasopressors. The vasodilatory state is mediated through adrenomedullin, calcitonin generelated peptide, nitric oxide, and other vasodilators, and is most pronounced in the splanchnic area. This constitutes an effective （although relative） counterbalance to increased arterial blood pressure. This review considers the alterations in systemic hemodynamics in patients with cirrhosis in relation to essential hypertension and arterial hypertension of the renal origin. Subjects with arterial hypertension （essential, secondary） may become normotensive during the development of cirrhosis, and arterial hypertension is rarely manifested in patients with cirrhosis, even in cases with renovascular disease and high circulating renin activity. There is much dispute as to the understanding of homoeostatic regulation in cirrhotic patients with manifest arterial hypertension. This most likely includes the combination of vasodilatation and vasoconstriction in parallel.
基金supported by the National Natural Science Foundation of China,No.81100856
文摘Acute brain injury caused by subarachnoid hemorrhage is the major cause of poor prognosis. The pathology of subarachnoid hemorrhage likely involves major morphological changes in the microcirculation. However, previous studies primarily used fixed tissue or delayed injury models. Therefore, in the present study, we used in vivo imaging to observe the dynamic changes in cerebral microcirculation after subarachnoid hemorrhage. Subarachnoid hemorrhage was induced by perforation of the bifurcation of the middle cerebral and anterior cerebral arteries in male C57/BL6 mice. The diameter of pial arterioles and venules was measured by in vivo fluorescence microscopy at different time points within 180 minutes after subarachnoid hemorrhage. Cerebral blood flow was examined and leukocyte adhesion/albumin extravasation was determined at different time points before and after subarachnoid hemorrhage. Cerebral pial microcirculation was abnormal and cerebral blood flow was reduced after subarachnoid hemorrhage. Acute vasoconstriction occurred predominantly in the arterioles instead of the venules. A progressive increase in the number of adherent leukocytes in venules and substantial albumin extravasation were observed between 10 and 180 minutes after subarachnoid hemorrhage. These results show that major changes in microcirculation occur in the early stage of subarachnoid hemorrhage. Our findings may promote the development of novel therapeutic strategies for the early treatment of subarachnoid hemorrhage.
文摘The influence of hypoxia on the activity of voltage-gated potassium channel in pulmonary artery smooth muscle cells （PASMCs） of rats and its roles in the pathogenesis of chronic pulmonary heart disease were investigated. Eighty male Sprague-Dawley rats were randomly allocated into control group （n=10）, acute hypoxic group （n=10）, and chronic hypoxic groups （n=60）. The chronic hypoxic groups were randomly divided into 6 subgroups （n=10 each） according to the chronic hypoxic periods. The rats in the control group were kept in room air and those in acute hypoxic group in hypoxia envi- ronmental chamber for 8 h. The rats in chronic hypoxic subgroups were kept in hypoxia environmental chamber for 8 h per day for 5, 10, 15, 20, 25, and 30 days, respectively. The mean pulmonary arterial pressure （mPAP）, right ventricular hypertrophy index （RVHI）, and the current of voltage-gated potas- sium channel （IK） in PASMCs were measured. Results showed that both acute and chronic hypoxia could decrease the IK in PASMCs of rats and the I-V relationship downward shifted to the right. And the peak Ir density at ＋60mV decreased with prolongation of hypoxia exposure. No significant difference was noted in the density oflK （at ＋60 mV） and I-V relationship between control group and chronic hy- poxic subgroup exposed to hypoxia for 5 days （P〉0.05）, but there was a significant difference between control group and chronic hypoxic subgroup exposed to hypoxia for 10 days （P〈0.05）. Significant dif- ferences were noted in the IK density （at ＋60 mV） and I-V relationships between control group and chronic hypoxic subgroups exposed to hypoxia for 20 days and 30 days （P〈0.01）. Compared with con- trol rats, the mPAP and RVHI were significantly increased after chronic exposure to hypoxia for 10 days （P〈0.05）, which were further increased with prolongation of hypoxia exposure, and there were signifi- cant differences between control group and chronic hypoxic subgroups exposed to hypoxia for 20 days and 30 days （P〈0.01）. Both the mPAP and the RVHI were negatively correlated with the density OflK （r---0.89769 and -0.94476, respectively, both P〈0.01）. It is concluded that exposure to hypoxia may cause decreased activity of voltage-gated potassium channel, leading to hypoxia pulmonary vasocon- striction （HPV）. Sustained HPV may result in chronic pulmonary hypertension, even chronic pulmonary heart disease, contributing to the pathogenesis of chronic pulmonary heart disease.
文摘Literature concerning procoagulant activity of the amniotic fluid and pathomechanism of amniotic fluid embolism (AFE) was surveyed and a new concept of its pathogenesis, called the integrated concept of AFE, was presented. According to this concept, two components of the amniotic fluid are involved: (i) apoptosis-affected amniotic cells showing a special role in the initiation of disseminated intravascular coagulation (DIC) and (ii) leukotrienes (formerly called slow-reacting substances), inducing bronchial and pulmonary vascular smooth muscle contraction. Although each of these components initiates a different pathogenic pathway, they both lead to the formation of a mechanical barrier on blood flow through the lungs (amniotic debris + microemboli) and/or functional barrier (pulmonary vasoconstriction). An old dilemma, concerning indications for heparin therapy in AFE was recalled in the light of the new concept.
基金Supported by The Profileringsfonds of the Maastricht University Medical Center(to Jacobs MJ and Buurman WA)an AGIKO-stipendium 920-03-522(to Lubbers T)from The Netherlands Organization for Health Research and Development
文摘AIM:To study the effect of circulating cell-free oxy-hemoglobin(FHb) on intestinal microcirculation and intestinal epithelial injury in a rat model. METHODS:To induce elevated intravascular circulating FHb,male Sprague-Dawley rats received water or FHb infusion.Microcirculatory changes in jejunum,ileum and colon were evaluated using fluorescent microspheres.Intestinal injury was quantified as plasmatic release of ileal lipid binding protein(iLBP) and verified by histological analysis of the ileum. RESULTS:Water and FHb infusions resulted,when compared with saline infusion,in reduced intestinal microcirculation(after 30 min P<0.05,or better;after 60 min FHb infusion P<0.05 for jejunum and colon) .Circulating FHb levels correlated significantly with release of iLBP(Spearman r=0.72,P=0.0011) .Epithelial cell injury of the villi was histologically observed after water and FHb infusions. CONCLUSION:This study shows that circulating FHb leads to a reduction in intestinal microcirculatory blood flow with marked injury to intestinal epithelial cells. These data support the hypothesis that circulating FHb contributes to the development of intestinal injury.
文摘The objective of this report is to describe the possible use of intramiometrial vasoconstrictive agents for laparoscopic management of interstitial pregnancy and the consequences in anatomical results and reproductive outcomes. Cornual resection can be performed by laparoscopy, but the high vascularization of this area may result in profuse bleeding and laparoscopic suturing under these conditions might be impossible for the majority of the surgeons. We present a case that describes the possible use of intramiometrial instillation of a solution of diluted epinephrine and levobupivacaine under laparoscopic guidance that permitted a bloodless cornual excision with complete reconstruction. Vasoactive agents might have potentially serious cardiovascular side effects and the correct election of the active principle and the dosage is essential to reduce the risk of the surgery and obtain good anatomical results and reproductive outcomes. In conclusion, unruptured interstitial pregnancies can be managed successfully with intramyometrial instillation of epinephrine and bupivacaine. This simple technique is particularly attractive as it facilitates anatomical reconstruction of the cornual area, gives enough time to perform a complete suture of the defect and reduces the risk of laparotomic conversion.
文摘Objecive To observe the eventual thermic effects of stimulaing Tàixī (太溪 KI 3) by telethermography. Methods Nine individuals of both sexes, chosen randomly, paricipated in this study. The temperature of the room where the experiment was carried out was not above 21 ℃. At the start of the experiment the volunteer stayed for exactly ten minutes in the room for acclimaizaion, then the first thermographic image was recorded for standardizaion purposes. Following this, an acupuncture needle was inserted at KI 3 only in the right leg, whose depth was limited to obtain Deqi, only manual stimulation for 15 min permanence in the site. Ater this period, new images were recorded. Results Significant reduction of all the right leg temperatures, by about 1.1 ℃ in all the volunteers that received the acupuncture at the Kl 3 was noted, with a coefficient variaion of P<0.0001 that was staisically highly significant, while on the other not simulated leg the variaion that occurred was around 0.7 ℃, with no significant coefficient variation of P>0.05. Conclusion The results of this study demonstrate that manual simulaion of the Kl 3 influences significantly peripheral vascular circulation, by means of sympathetic stimulaion causing vasoconstricion.
