[Objectives]The aim of this study was to investigate the effect of electroacupuncture on infarct size in cerebral ischemic stroke.[Methods]A systematic electronic search was conducted up to June 1,2024.TTC staining wa...[Objectives]The aim of this study was to investigate the effect of electroacupuncture on infarct size in cerebral ischemic stroke.[Methods]A systematic electronic search was conducted up to June 1,2024.TTC staining was used to evaluate the infarct size.Standard mean differences(SMD)with a95%confidence interval(CI)were calculated to assess the two intervention methods.The heterogeneity of the included studies was also tested.Two analyses with subgroups were planned:intervention start time(before MCAOversus after MCAO).waveform(continuous wave versus disperse wave).[Results]Forty-one studies with a total of 502 rats or mice were included in this review.The pooled analysis of these trials showed a significant positive effect of electroacupuncture on the infarct size(SMD=-2.65,P<0.0001,Z=12.55).Subgroup analysis results indicated that electroacupuncture intervention before MCAO surgery(16 studies,SMD=-2.73,P<0.00001,Z=10.60)could more significantly reduce infarct size than that after MCAO surgery(25studies,SMD=-2.61,P<0.00001,Z=8.20).Additionally,disperse waves(31 studies,SMD=-2.46,P<0.00001,Z=11.08)were more effective in reducing infarct area than continuous waves(10 studies,SMD=-3.38,P<0.00001,Z=6.12).[Conclusions]This review provided sufficient evidence that electroacupuncture before MCAO surgery with disperse waves was more effective in reducing infarct area than after MCAO surgery and continu-ous waves.展开更多
Previous studies have shown that nicorandil has a protective effect on cardiomyocytes.However,there is no study to investigate whether perioperative intravenous nicorandil can further reduce the myocardial infarct siz...Previous studies have shown that nicorandil has a protective effect on cardiomyocytes.However,there is no study to investigate whether perioperative intravenous nicorandil can further reduce the myocardial infarct size in patients with ST-segment elevation myocardial infarction(STEMI)compared to the current standard of percutaneous coronary intervention(PCI)regimen.The CHANGE(China-Administration of Nicorandil Group)study is a multicenter,prospective,randomized,double-blind and parallel-controlled clinical study of STEMI patients undergoing primary PCI in China,aiming to evaluate the efficacy and safety of intravenous nicorandil in ameliorating the myocardial infarct size in STEMI patients undergoing primary PCI and provide evidence-based support for myocardial protection strategies of STEMI patients.展开更多
AIM To evaluate the effects of glucagon-like peptide-1 analogs(GLP-1 a) combined with insulin on myocardial ischemiareperfusion injury in diabetic rats.METHODS Type 2 diabetes mellitus(T2 DM) was induced in maleWistar...AIM To evaluate the effects of glucagon-like peptide-1 analogs(GLP-1 a) combined with insulin on myocardial ischemiareperfusion injury in diabetic rats.METHODS Type 2 diabetes mellitus(T2 DM) was induced in maleWistar rats with streptozotocin(65 mg/kg) and verified using an oral glucose tolerance test. After anesthesia, the left coronary artery was occluded for 40 min followed by 80 min reperfusion. Blood glucose level was measured during surgery. Rats were randomized into six groups as follows:(1) control rats;(2) insulin(0.1 U/kg) treated rats prior to ischemia;(3) insulin(0.1 U/kg) treated rats at reperfusion;(4) GLP-1 a(140 mg/kg) treated rats prior to ischemia;(5) GLP-1 a(140 mg/kg) treated rats at reperfusion; and(6) rats treated with GLP-1 a(140 mg/kg) prior to ischemia plus insulin(0.1 U/kg) at reperfusion. Myocardial area at risk and infarct size was measured planimetrically using Evans blue and triphenyltetrazolium chloride staining, respectively.RESULTS There was no significant difference in the myocardial area at risk among groups. Insulin treatment before ischemia resulted in a significant increase in infarct size(34.7% ± 3.4% vs 18.6% ± 3.1% in the control rats, P < 0.05). Post-ischemic administration of insulin or GLP-1 a had no effect on infarct size. However, pre-ischemic administration of GLP-1 a reduced infarct size to 12% ± 2.2%(P < 0.05). The maximal infarct size reduction was observed in the group treated with GLP-1 a prior to ischemia and insulin at reperfusion(8% ± 1.6%, P < 0.05 vs the control and GLP-1 a alone treated groups).CONCLUSION GLP-1 a pre-administration results in myocardial infarct size reduction in rats with T2 DM. These effects are maximal in rats treated with GLP-1 a pre-ischemia plus insulin at reperfusion.展开更多
Tumour necrosis factor-α is a cytokine released during myocardial infarction. According to the literature, the effect of TNFα on myocardial infarction is controversial, especially when administered before the ischem...Tumour necrosis factor-α is a cytokine released during myocardial infarction. According to the literature, the effect of TNFα on myocardial infarction is controversial, especially when administered before the ischemic period. The deleterious effects of TNFα seem to be related to the triggering of apoptosis. This study has been designed to determine if different doses of TNFα, administered before the ischemic period, have the same effect on infarct size and on activation of caspase-3 and-8, two enzymes involved in apoptosis. Four groups, using a porcine model of myocardial infarction, have been used: placebo and TNFα (0.1 μg/kg;1 μg/kg and 3 μg/kg). All administered 15 minutes before a 50 minutes occlusion of the left anterior descending artery. Myocardial infarct size has been determined at 3 hours of reperfusion. In a subgroup of animals, reperfusion period has been limited to 15 min to determine the activity of caspase-3 and-8 by spectrofluorometry. Results indicated that infarct size is significantly smaller in groups 0.1 μg/kg and 1 μg/ kg as compared to the placebo group. In contrast, the 3 μg/kg group presented an infarct size similar to the placebo group. Activity of caspase-3 and-8 is reduced in the ischemic region in groups 0.1 and 1 μg/ kg as compared to the placebo group whereas activity in the 3 μg/kg group was similar to the placebo. The results obtained indicated that a low dose of TNFα administered before the ischemic period reduces infarct size, whereas the cardioprotection is lost with the high dose.展开更多
Background The definitive treatment for myocardial ischemia is reperfusion. However, reperfusion injury has the potential to cause additional reversible and irreversible damage to the myocardium. One likely candidate ...Background The definitive treatment for myocardial ischemia is reperfusion. However, reperfusion injury has the potential to cause additional reversible and irreversible damage to the myocardium. One likely candidate for a cardioprotection is adenosine. The present study aimed at investigating the effect of intravenous adenosine on clinical outcomes in patients with ST-segment elevation myocardial infarction （STEMI） undergoing primary percutaneous coronary intervention （PCI）. Methods Patients with STEMI within 12 hours from the onset of symptoms were randomized by 1：1：1 ratio to receive either adenosine 50μg-kg-1.min-1 （low-dose group, n=31）, or 70 μg.kg-1.min1 （high-dose group, n=32）, or saline 1 ml/min （control group, n=27） for three hours. Drugs were given to the patients immediately after the guide wire crossed the culprit lesion. Recurrence of no-reflow, TIMI flow grade （TFG） and TIMI myocardial perfusion grade （TMPG）, and collateral circulation were recorded. The postoperative and preoperative ST segment elevation sum of 18-lead electrocardiogram （ECG） and their ratio （STsum-post/STsum-pre） were recorded, as well as the peak time and peak value of CK-MB enzyme. Serial cardiac echo and myocardial perfusion imaging were performed at 24 hours and 6 months post-stenting. The primary endpoint was left ventricular function, and infarct size. The secondary end-point was the occurrence of cardiac and non-cardiac death, non-fatal myocardial infarction, and heart failure. Results A total of 90 STEMI patients were studied. No-reflow immediately after stent procedure was seen in 11 （35.5%） patients in the control group, significantly different from 6.3% in the low-dose group or 3.7% in the high-dose group （both P=0.001）. STsum-post/STsum-pre in the low-dose and high-dose groups was significantly different from the control group （low-dose group vs. control group, P=0.003 and high-dose group vs. control group, P=0.001）, without a dose-dependent pattern （P=0.238）. The peak value of CK-MB enzyme was significantly reduced in the high-dose group compared to the control group （P=-0.024）. Compared to the left ventricular ejection fraction （LVEF） in control group, LVEF in the low-dose group increased by 5.8% at 24 hours （P=0.012） and by 10.9% at 6 months （P=0,007）, LVEF in the high-dose group increased by 9.5% at 24 hours （P=0.001） and by 10.0% at 6 months （P=0.001）, respectively. Significant reduction of infarct size by 24.2% was detected in the high-dose group vs. low-dose or control groups （P=0.008）. There was no significant difference regarding secondary endpoints at 6 months among the treated groups. Cardiac function by NYHA classification in both the low-dose and the high-dose groups was improved significantly （P=0.013, P=0.016）. Conclusion Intravenous adenosine administration might significantly reduce the recurrence of no-reflow, with resultant improved left ventricular systolic function. High-dose adenosine was further associated with significant reduction of infarct size.展开更多
BACKGROUND:Intravenous transplantation has been regarded as a most safe method in stem cell therapies.There is evidence showing the homing of bone marrow stem cells(BMSCs) into the injured sites,and thus these cells c...BACKGROUND:Intravenous transplantation has been regarded as a most safe method in stem cell therapies.There is evidence showing the homing of bone marrow stem cells(BMSCs) into the injured sites,and thus these cells can be used in the treatment of acute myocardial infarction(Ml).This study aimed to investigate the effect of intravenous and epicardial transplantion of BMSCs on myocardial infarction size in a rabbit model.METHODS:A total of 60 New Zealand rabbits were randomly divided into three groups:control group,epicardium group(group Ⅰ) and ear vein group(group Ⅱ).The BMSCs were collected from the tibial plateau in group Ⅰ and group Ⅱ,cultured and labeled.In the three groups,rabbits underwent thoracotomy and ligation of the middle left anterior descending artery.The elevation of ST segment>0.2 mV lasting for 30 minutes on the lead Ⅱ and Ⅲ of electrocardiogram suggested successful introduction of myocardial infarction.Two weeks after myocardial infarction,rabbits in group Ⅰ were treated with autogenous BMSCs at the infarct region and those in group Ⅱ received intravenous transplantation of BMSCs.In the control group,rabbits were treated with PBS following thoracotomy.Four weeks after myocardial infarction,the heart was collected from all rabbits and the infarct size was calculated.The heart was cut into sections followed by HE staining and calculation of infarct size with an image system.RESULTS:In groups Ⅰ and Ⅱ,the infarct size was significantly reduced after transplantation with BMSCs when compared with the control group(P<0.05).However,there was no significant difference in the infarct size between groups Ⅰ and Ⅱ(P>0.05).CONCLUSION:Transplantation of BMSCs has therapeutic effect on Ml.Moreover,epicardial and intravenous transplantation of BMSCs has comparable therapeutic efficacy on myocardial infarction.展开更多
The contribution of the inhibition of angiotensin Ⅱ (ANGⅡ) synthesis and bradykinin (BK) breakdown to the effects of ACE inhibition on infarct size, cardiac hypertrophy and blood supply to the marginal zone of the i...The contribution of the inhibition of angiotensin Ⅱ (ANGⅡ) synthesis and bradykinin (BK) breakdown to the effects of ACE inhibition on infarct size, cardiac hypertrophy and blood supply to the marginal zone of the infarcted area展开更多
This study sought to examine neuroglobin （NGB） in the serum of acute cerebral infarction patients with double-antibody sandwich enzyme-linked immunosorbent assay to identify all risk factors, calculate infarct size,...This study sought to examine neuroglobin （NGB） in the serum of acute cerebral infarction patients with double-antibody sandwich enzyme-linked immunosorbent assay to identify all risk factors, calculate infarct size, assess neurological impairment, and analyze the relation between NGB and each of these factors. The double-antibody sandwich assay indicated that levels of NGB in serum were unaltered within 6 hours following acute cerebral infarction compared with normal levels. NGB levels then underwent a distinct change, peaking at 24 hours then returning to normal levels in 72 hours. The results suggest that the level of NGB might be related to infarct size and low-density lipoprotein at 24 hours after acute cerebral infarction. There were no significant differences in neurological impairment scores and infarct size at different periods following infarction. The findings indicated that the level of NGB in serum of acute cerebral infarction patients was correlated with infarct time.展开更多
Objective Previous studies showed that hypoxia preconditioning could protect cardiac function against subsequent myo-cardial infarction injury. However, the effect of hypoxia on left ventricular after myocardial infar...Objective Previous studies showed that hypoxia preconditioning could protect cardiac function against subsequent myo-cardial infarction injury. However, the effect of hypoxia on left ventricular after myocardial infarction is still unclear. This study therefore aims to investigate the effects of hypoxia training on left ventricular remodeling in rabbits post myocardial infarction. Methods Adult male rabbits were randomly divided into three groups： group SO （sham operated）, group MI （myocardial infarc-tion only） and group MI-HT （myocardial infarction plus hypoxia training）. Myocardial infarction was induced by left ventricular branch ligation. Hypoxia training was performed in a hypobaric chamber （having equivalent condition at an altitude of 4000 m, FiO214.9%） for 1 h/day, 5 days/week for four weeks. At the endpoints, vascular endothelial growth factor （VEGF） in the plasma was measured. Infarct size and capillary density were detected by histology. Left ventricular remodeling and function were as-sessed by echocardiography.Results After the 4-week experiment, compared with the group SO, plasma VEGF levels in groups MI （130.27 ± 18.58 pg/mL,P〈 0.01） and MI-HT （181.93 ± 20.29 pg/mL,P〈 0.01） were significantly increased. Infarct size in Group MI-HT （29.67% ± 7.73%） was deceased remarkably, while its capillary density （816.0 ± 122.2/mm2） was significantly increased. For both groups MI and MI-HT, left ventricular end-diastolic and end-systolic dimensions were increased whereas left ventricular ejection fraction was decreased. However, compared with group MI, group MI-HT diminished left ventricular end-diastolic （15.86 ± 1.09 mm,P〈 0.05） and end-systolic dimensions （12.10 ± 1.20 mm,P〈 0.01） significantly and im-proved left ventricular ejection fraction （54.39 ± 12.74 mm,P〈 0.05）.ConclusionHypoxia training may improve left ven-tricular function and reduce remodeling via angiogenesis in rabbits with MI.展开更多
Objective:To investigate the effects of butylphthalide on reducing neuronal apoptosis in rats with cerebral infarction by inhibiting the JNK/P38 MAPK signaling pathway.Methods:Forty-eight SD male rats were divided int...Objective:To investigate the effects of butylphthalide on reducing neuronal apoptosis in rats with cerebral infarction by inhibiting the JNK/P38 MAPK signaling pathway.Methods:Forty-eight SD male rats were divided into DZ group(control group),CI group(model group)and NBP group(butylphthalide group).Rats in CI group and NBP group were used to establish cerebral infarction models.NBP group used NBP.The solution(80 mg/(kg?d))was administered orally,and the remaining two groups were administered with the same volume of peanut oil.After 14 consecutive days of treatment,the Zea Longa score was used to evaluate the neurological function of DZ,CI and NBP rats.Scoring,TTC staining was used to observe the cerebral infarction volume of rats in DZ group,CI group and NBP group,HE staining was used to observe the pathological morphology of brain tissue in DZ group,CI group and NBP group.Neuronal apoptosis,Western blot was used to detect the expression of p-JNK and p-p38MAPK in brain tissues of DZ group,CI group and NBP group.Results:The neurological function of the rats in the CI group was higher than that in the DZ group,and the difference was statistically significant(P<0.05).The neurological function score of the rats in the NBP group was reduced compared with the CI group,and the difference was statistically significant(P<0.05).The cerebral infarction volume in the group was 35.56%higher than that in the DZ group,and the difference was statistically significant(P<0.05).The minor infarct volume in the NBP group was 21.59%,which was less than that in the CI group,and the difference was statistically significant(P<0.05).Nerve cells are neatly sorted,with a large number.The gap between blood vessels and interstitial tissue in the CI group is enlarged,the cells are severely contracted,and the neuron structure is incomplete.Compared with the CI group,the NBP group has reduced neuron contraction and increased number;The dead nerve cells were brown.The apoptosis rate of nerve cells in the CI group was 79.65%higher than that in the DZ group was 5.82%.The difference was statistically significant(P<0.05).The nerve cell apoptosis rate in the NBP group was 30.23%.Compared with CI group,the difference was statistically significant(P<0.05);Western blot results showed that p-JNK and p-p38MAPK protein expression in CI group was higher than that in DZ group,and the difference was statistically significant(P<0.05).The levels of p-JNK and p-p38MAPK proteins in the NBP group were lower than those in the CI group.There was statistically significant(P<0.05).Conclusion:Butylphthalide can improve neurological damage,reduce apoptotic nerve cells,and reduce infarct volume in rats with cerebral infarction,which is related to the inhibition of JNK/P38 MAPK pathway expression.展开更多
In patients with an acute ST-segment elevation myocardial infarction, timely myocardial reperfusion using primary percutaneous coronary intervention is the most effective therapy for limiting myocardial infarct size, ...In patients with an acute ST-segment elevation myocardial infarction, timely myocardial reperfusion using primary percutaneous coronary intervention is the most effective therapy for limiting myocardial infarct size, preserving left-ventricular systolic function and reducing the onset of heart failure. Within minutes after the restoration of blood flow, however, reperfusion itself results in additional damage, also known as myocardial ischemia-reperfusion injury. An improved understanding of the pathophysiological mechanisms underlying reperfusion injury has resulted in the identification ofseveral promising pharmacological(cyclosporin-A, exenatide, glucose-insulin-potassium, atrial natriuretic peptide, adenosine, abciximab, erythropoietin, metoprolol and melatonin) therapeutic strategies for reducing the severity of myocardial reperfusion injury. Many of these agents have shown promise in initial proofof-principle clinical studies. In this article, we review the pathophysiology underlying myocardial reperfusion injury and highlight the potential pharmacological interventions which could be used in the future to prevent reperfusion injury and improve clinical outcomes in patients with coronary heart disease.展开更多
The acute myocardial infarction(AMI)and sudden cardiac death(SCD),both associated with acute cardiac ischemia,are one of the leading causes of adult death in economically developed countries.The development of new app...The acute myocardial infarction(AMI)and sudden cardiac death(SCD),both associated with acute cardiac ischemia,are one of the leading causes of adult death in economically developed countries.The development of new approaches for the treatment and prevention of AMI and SCD remains the highest priority for medicine.A study on the cardiovascular effects of chronic hypoxia(CH)may contribute to the development of these methods.Chronic hypoxia exerts both positive and adverse effects.The positive effects are the infarct-reducing,vasoprotective,and antiarrhythmic effects,which can lead to the improvement of cardiac contractility in reperfusion.The adverse effects are pulmonary hypertension and right ventricular hypertrophy.This review presents a comprehensive overview of how CH enhances cardiac tolerance to ischemia/reperfusion.It is an in-depth analysis of the published data on the underlying mechanisms,which can lead to future development of the cardioprotective effect of CH.A better understanding of the CH-activated protective signaling pathways may contribute to new therapeutic approaches in an increase of cardiac tolerance to ischemia/reperfusion.展开更多
Primary coronary revascularization by means of percutaneous coronary intervention(PCI)is a highly effective treatment of acute myocardial infarction re-establishing coronary perfusion and stopping the ongoing necrosis...Primary coronary revascularization by means of percutaneous coronary intervention(PCI)is a highly effective treatment of acute myocardial infarction re-establishing coronary perfusion and stopping the ongoing necrosis in the dependent myocardium.Single-photon emission computed tomography(SPECT)is the most widely used modality assessing myocardial salvage as the difference between the acute perfusion defect before intervention and the remaining scar size measured in a second scan several days after the event.SPECT allows quantification of area at risk(AAR)and final infarct size(FIS)by tracer injection prior to revascularization and after 1 month,respectively.SPECT provides the most validated measure of myocardial salvage and has been utilized in multiple randomizedclinical trials.However,SPECT is logistically challenging,expensive,and includes radiation exposure.More recently,a large number of studies have suggested that cardiac magnetic resonance(CMR)can determine salvage in a single examination by combining measures of myocardial oedema in the AAR exposed to ischaemia reperfusion with FIS quantification by late gadolinium enhancement.展开更多
文摘[Objectives]The aim of this study was to investigate the effect of electroacupuncture on infarct size in cerebral ischemic stroke.[Methods]A systematic electronic search was conducted up to June 1,2024.TTC staining was used to evaluate the infarct size.Standard mean differences(SMD)with a95%confidence interval(CI)were calculated to assess the two intervention methods.The heterogeneity of the included studies was also tested.Two analyses with subgroups were planned:intervention start time(before MCAOversus after MCAO).waveform(continuous wave versus disperse wave).[Results]Forty-one studies with a total of 502 rats or mice were included in this review.The pooled analysis of these trials showed a significant positive effect of electroacupuncture on the infarct size(SMD=-2.65,P<0.0001,Z=12.55).Subgroup analysis results indicated that electroacupuncture intervention before MCAO surgery(16 studies,SMD=-2.73,P<0.00001,Z=10.60)could more significantly reduce infarct size than that after MCAO surgery(25studies,SMD=-2.61,P<0.00001,Z=8.20).Additionally,disperse waves(31 studies,SMD=-2.46,P<0.00001,Z=11.08)were more effective in reducing infarct area than continuous waves(10 studies,SMD=-3.38,P<0.00001,Z=6.12).[Conclusions]This review provided sufficient evidence that electroacupuncture before MCAO surgery with disperse waves was more effective in reducing infarct area than after MCAO surgery and continu-ous waves.
基金supported by the National Key Research and Development program of China(2018ZX09201013)Xinxin Merck Cardiovascular Research Fund(2017-CCA-xinxin merck fund-003)。
文摘Previous studies have shown that nicorandil has a protective effect on cardiomyocytes.However,there is no study to investigate whether perioperative intravenous nicorandil can further reduce the myocardial infarct size in patients with ST-segment elevation myocardial infarction(STEMI)compared to the current standard of percutaneous coronary intervention(PCI)regimen.The CHANGE(China-Administration of Nicorandil Group)study is a multicenter,prospective,randomized,double-blind and parallel-controlled clinical study of STEMI patients undergoing primary PCI in China,aiming to evaluate the efficacy and safety of intravenous nicorandil in ameliorating the myocardial infarct size in STEMI patients undergoing primary PCI and provide evidence-based support for myocardial protection strategies of STEMI patients.
基金Supported by Russian Science Foundation,No.17-75-30052
文摘AIM To evaluate the effects of glucagon-like peptide-1 analogs(GLP-1 a) combined with insulin on myocardial ischemiareperfusion injury in diabetic rats.METHODS Type 2 diabetes mellitus(T2 DM) was induced in maleWistar rats with streptozotocin(65 mg/kg) and verified using an oral glucose tolerance test. After anesthesia, the left coronary artery was occluded for 40 min followed by 80 min reperfusion. Blood glucose level was measured during surgery. Rats were randomized into six groups as follows:(1) control rats;(2) insulin(0.1 U/kg) treated rats prior to ischemia;(3) insulin(0.1 U/kg) treated rats at reperfusion;(4) GLP-1 a(140 mg/kg) treated rats prior to ischemia;(5) GLP-1 a(140 mg/kg) treated rats at reperfusion; and(6) rats treated with GLP-1 a(140 mg/kg) prior to ischemia plus insulin(0.1 U/kg) at reperfusion. Myocardial area at risk and infarct size was measured planimetrically using Evans blue and triphenyltetrazolium chloride staining, respectively.RESULTS There was no significant difference in the myocardial area at risk among groups. Insulin treatment before ischemia resulted in a significant increase in infarct size(34.7% ± 3.4% vs 18.6% ± 3.1% in the control rats, P < 0.05). Post-ischemic administration of insulin or GLP-1 a had no effect on infarct size. However, pre-ischemic administration of GLP-1 a reduced infarct size to 12% ± 2.2%(P < 0.05). The maximal infarct size reduction was observed in the group treated with GLP-1 a prior to ischemia and insulin at reperfusion(8% ± 1.6%, P < 0.05 vs the control and GLP-1 a alone treated groups).CONCLUSION GLP-1 a pre-administration results in myocardial infarct size reduction in rats with T2 DM. These effects are maximal in rats treated with GLP-1 a pre-ischemia plus insulin at reperfusion.
文摘Tumour necrosis factor-α is a cytokine released during myocardial infarction. According to the literature, the effect of TNFα on myocardial infarction is controversial, especially when administered before the ischemic period. The deleterious effects of TNFα seem to be related to the triggering of apoptosis. This study has been designed to determine if different doses of TNFα, administered before the ischemic period, have the same effect on infarct size and on activation of caspase-3 and-8, two enzymes involved in apoptosis. Four groups, using a porcine model of myocardial infarction, have been used: placebo and TNFα (0.1 μg/kg;1 μg/kg and 3 μg/kg). All administered 15 minutes before a 50 minutes occlusion of the left anterior descending artery. Myocardial infarct size has been determined at 3 hours of reperfusion. In a subgroup of animals, reperfusion period has been limited to 15 min to determine the activity of caspase-3 and-8 by spectrofluorometry. Results indicated that infarct size is significantly smaller in groups 0.1 μg/kg and 1 μg/ kg as compared to the placebo group. In contrast, the 3 μg/kg group presented an infarct size similar to the placebo group. Activity of caspase-3 and-8 is reduced in the ischemic region in groups 0.1 and 1 μg/ kg as compared to the placebo group whereas activity in the 3 μg/kg group was similar to the placebo. The results obtained indicated that a low dose of TNFα administered before the ischemic period reduces infarct size, whereas the cardioprotection is lost with the high dose.
文摘Background The definitive treatment for myocardial ischemia is reperfusion. However, reperfusion injury has the potential to cause additional reversible and irreversible damage to the myocardium. One likely candidate for a cardioprotection is adenosine. The present study aimed at investigating the effect of intravenous adenosine on clinical outcomes in patients with ST-segment elevation myocardial infarction （STEMI） undergoing primary percutaneous coronary intervention （PCI）. Methods Patients with STEMI within 12 hours from the onset of symptoms were randomized by 1：1：1 ratio to receive either adenosine 50μg-kg-1.min-1 （low-dose group, n=31）, or 70 μg.kg-1.min1 （high-dose group, n=32）, or saline 1 ml/min （control group, n=27） for three hours. Drugs were given to the patients immediately after the guide wire crossed the culprit lesion. Recurrence of no-reflow, TIMI flow grade （TFG） and TIMI myocardial perfusion grade （TMPG）, and collateral circulation were recorded. The postoperative and preoperative ST segment elevation sum of 18-lead electrocardiogram （ECG） and their ratio （STsum-post/STsum-pre） were recorded, as well as the peak time and peak value of CK-MB enzyme. Serial cardiac echo and myocardial perfusion imaging were performed at 24 hours and 6 months post-stenting. The primary endpoint was left ventricular function, and infarct size. The secondary end-point was the occurrence of cardiac and non-cardiac death, non-fatal myocardial infarction, and heart failure. Results A total of 90 STEMI patients were studied. No-reflow immediately after stent procedure was seen in 11 （35.5%） patients in the control group, significantly different from 6.3% in the low-dose group or 3.7% in the high-dose group （both P=0.001）. STsum-post/STsum-pre in the low-dose and high-dose groups was significantly different from the control group （low-dose group vs. control group, P=0.003 and high-dose group vs. control group, P=0.001）, without a dose-dependent pattern （P=0.238）. The peak value of CK-MB enzyme was significantly reduced in the high-dose group compared to the control group （P=-0.024）. Compared to the left ventricular ejection fraction （LVEF） in control group, LVEF in the low-dose group increased by 5.8% at 24 hours （P=0.012） and by 10.9% at 6 months （P=0,007）, LVEF in the high-dose group increased by 9.5% at 24 hours （P=0.001） and by 10.0% at 6 months （P=0.001）, respectively. Significant reduction of infarct size by 24.2% was detected in the high-dose group vs. low-dose or control groups （P=0.008）. There was no significant difference regarding secondary endpoints at 6 months among the treated groups. Cardiac function by NYHA classification in both the low-dose and the high-dose groups was improved significantly （P=0.013, P=0.016）. Conclusion Intravenous adenosine administration might significantly reduce the recurrence of no-reflow, with resultant improved left ventricular systolic function. High-dose adenosine was further associated with significant reduction of infarct size.
基金supported by grants from the Scientific Research Plan Project of Liaoning Province(20092250096)Scientific Research Plan Project of Dalian(2010E15SF178)
文摘BACKGROUND:Intravenous transplantation has been regarded as a most safe method in stem cell therapies.There is evidence showing the homing of bone marrow stem cells(BMSCs) into the injured sites,and thus these cells can be used in the treatment of acute myocardial infarction(Ml).This study aimed to investigate the effect of intravenous and epicardial transplantion of BMSCs on myocardial infarction size in a rabbit model.METHODS:A total of 60 New Zealand rabbits were randomly divided into three groups:control group,epicardium group(group Ⅰ) and ear vein group(group Ⅱ).The BMSCs were collected from the tibial plateau in group Ⅰ and group Ⅱ,cultured and labeled.In the three groups,rabbits underwent thoracotomy and ligation of the middle left anterior descending artery.The elevation of ST segment>0.2 mV lasting for 30 minutes on the lead Ⅱ and Ⅲ of electrocardiogram suggested successful introduction of myocardial infarction.Two weeks after myocardial infarction,rabbits in group Ⅰ were treated with autogenous BMSCs at the infarct region and those in group Ⅱ received intravenous transplantation of BMSCs.In the control group,rabbits were treated with PBS following thoracotomy.Four weeks after myocardial infarction,the heart was collected from all rabbits and the infarct size was calculated.The heart was cut into sections followed by HE staining and calculation of infarct size with an image system.RESULTS:In groups Ⅰ and Ⅱ,the infarct size was significantly reduced after transplantation with BMSCs when compared with the control group(P<0.05).However,there was no significant difference in the infarct size between groups Ⅰ and Ⅱ(P>0.05).CONCLUSION:Transplantation of BMSCs has therapeutic effect on Ml.Moreover,epicardial and intravenous transplantation of BMSCs has comparable therapeutic efficacy on myocardial infarction.
文摘The contribution of the inhibition of angiotensin Ⅱ (ANGⅡ) synthesis and bradykinin (BK) breakdown to the effects of ACE inhibition on infarct size, cardiac hypertrophy and blood supply to the marginal zone of the infarcted area
基金the Science and Technology Plan of Anhui Province, No.08020304111
文摘This study sought to examine neuroglobin （NGB） in the serum of acute cerebral infarction patients with double-antibody sandwich enzyme-linked immunosorbent assay to identify all risk factors, calculate infarct size, assess neurological impairment, and analyze the relation between NGB and each of these factors. The double-antibody sandwich assay indicated that levels of NGB in serum were unaltered within 6 hours following acute cerebral infarction compared with normal levels. NGB levels then underwent a distinct change, peaking at 24 hours then returning to normal levels in 72 hours. The results suggest that the level of NGB might be related to infarct size and low-density lipoprotein at 24 hours after acute cerebral infarction. There were no significant differences in neurological impairment scores and infarct size at different periods following infarction. The findings indicated that the level of NGB in serum of acute cerebral infarction patients was correlated with infarct time.
基金We are grateful to the support of Dr. Lei Yuan and Shao-Shao Zhao for their technical assistance. This work was supported in part by China Postdoctoral Science Foundation Province, China
文摘Objective Previous studies showed that hypoxia preconditioning could protect cardiac function against subsequent myo-cardial infarction injury. However, the effect of hypoxia on left ventricular after myocardial infarction is still unclear. This study therefore aims to investigate the effects of hypoxia training on left ventricular remodeling in rabbits post myocardial infarction. Methods Adult male rabbits were randomly divided into three groups： group SO （sham operated）, group MI （myocardial infarc-tion only） and group MI-HT （myocardial infarction plus hypoxia training）. Myocardial infarction was induced by left ventricular branch ligation. Hypoxia training was performed in a hypobaric chamber （having equivalent condition at an altitude of 4000 m, FiO214.9%） for 1 h/day, 5 days/week for four weeks. At the endpoints, vascular endothelial growth factor （VEGF） in the plasma was measured. Infarct size and capillary density were detected by histology. Left ventricular remodeling and function were as-sessed by echocardiography.Results After the 4-week experiment, compared with the group SO, plasma VEGF levels in groups MI （130.27 ± 18.58 pg/mL,P〈 0.01） and MI-HT （181.93 ± 20.29 pg/mL,P〈 0.01） were significantly increased. Infarct size in Group MI-HT （29.67% ± 7.73%） was deceased remarkably, while its capillary density （816.0 ± 122.2/mm2） was significantly increased. For both groups MI and MI-HT, left ventricular end-diastolic and end-systolic dimensions were increased whereas left ventricular ejection fraction was decreased. However, compared with group MI, group MI-HT diminished left ventricular end-diastolic （15.86 ± 1.09 mm,P〈 0.05） and end-systolic dimensions （12.10 ± 1.20 mm,P〈 0.01） significantly and im-proved left ventricular ejection fraction （54.39 ± 12.74 mm,P〈 0.05）.ConclusionHypoxia training may improve left ven-tricular function and reduce remodeling via angiogenesis in rabbits with MI.
基金Key research project of medical science of Hubei province
文摘Objective:To investigate the effects of butylphthalide on reducing neuronal apoptosis in rats with cerebral infarction by inhibiting the JNK/P38 MAPK signaling pathway.Methods:Forty-eight SD male rats were divided into DZ group(control group),CI group(model group)and NBP group(butylphthalide group).Rats in CI group and NBP group were used to establish cerebral infarction models.NBP group used NBP.The solution(80 mg/(kg?d))was administered orally,and the remaining two groups were administered with the same volume of peanut oil.After 14 consecutive days of treatment,the Zea Longa score was used to evaluate the neurological function of DZ,CI and NBP rats.Scoring,TTC staining was used to observe the cerebral infarction volume of rats in DZ group,CI group and NBP group,HE staining was used to observe the pathological morphology of brain tissue in DZ group,CI group and NBP group.Neuronal apoptosis,Western blot was used to detect the expression of p-JNK and p-p38MAPK in brain tissues of DZ group,CI group and NBP group.Results:The neurological function of the rats in the CI group was higher than that in the DZ group,and the difference was statistically significant(P<0.05).The neurological function score of the rats in the NBP group was reduced compared with the CI group,and the difference was statistically significant(P<0.05).The cerebral infarction volume in the group was 35.56%higher than that in the DZ group,and the difference was statistically significant(P<0.05).The minor infarct volume in the NBP group was 21.59%,which was less than that in the CI group,and the difference was statistically significant(P<0.05).Nerve cells are neatly sorted,with a large number.The gap between blood vessels and interstitial tissue in the CI group is enlarged,the cells are severely contracted,and the neuron structure is incomplete.Compared with the CI group,the NBP group has reduced neuron contraction and increased number;The dead nerve cells were brown.The apoptosis rate of nerve cells in the CI group was 79.65%higher than that in the DZ group was 5.82%.The difference was statistically significant(P<0.05).The nerve cell apoptosis rate in the NBP group was 30.23%.Compared with CI group,the difference was statistically significant(P<0.05);Western blot results showed that p-JNK and p-p38MAPK protein expression in CI group was higher than that in DZ group,and the difference was statistically significant(P<0.05).The levels of p-JNK and p-p38MAPK proteins in the NBP group were lower than those in the CI group.There was statistically significant(P<0.05).Conclusion:Butylphthalide can improve neurological damage,reduce apoptotic nerve cells,and reduce infarct volume in rats with cerebral infarction,which is related to the inhibition of JNK/P38 MAPK pathway expression.
基金Supported by Framework of one research project of the Spanish Society of Cardiology for Clinical Research in Cardiology 2012
文摘In patients with an acute ST-segment elevation myocardial infarction, timely myocardial reperfusion using primary percutaneous coronary intervention is the most effective therapy for limiting myocardial infarct size, preserving left-ventricular systolic function and reducing the onset of heart failure. Within minutes after the restoration of blood flow, however, reperfusion itself results in additional damage, also known as myocardial ischemia-reperfusion injury. An improved understanding of the pathophysiological mechanisms underlying reperfusion injury has resulted in the identification ofseveral promising pharmacological(cyclosporin-A, exenatide, glucose-insulin-potassium, atrial natriuretic peptide, adenosine, abciximab, erythropoietin, metoprolol and melatonin) therapeutic strategies for reducing the severity of myocardial reperfusion injury. Many of these agents have shown promise in initial proofof-principle clinical studies. In this article, we review the pathophysiology underlying myocardial reperfusion injury and highlight the potential pharmacological interventions which could be used in the future to prevent reperfusion injury and improve clinical outcomes in patients with coronary heart disease.
基金supported by the Russian Science Foundation grant 22-15-00048The section dedicated to the role of kinases in the cardioprotective effect of CH is framed within the framework of state assignments 122020300042-4.
文摘The acute myocardial infarction(AMI)and sudden cardiac death(SCD),both associated with acute cardiac ischemia,are one of the leading causes of adult death in economically developed countries.The development of new approaches for the treatment and prevention of AMI and SCD remains the highest priority for medicine.A study on the cardiovascular effects of chronic hypoxia(CH)may contribute to the development of these methods.Chronic hypoxia exerts both positive and adverse effects.The positive effects are the infarct-reducing,vasoprotective,and antiarrhythmic effects,which can lead to the improvement of cardiac contractility in reperfusion.The adverse effects are pulmonary hypertension and right ventricular hypertrophy.This review presents a comprehensive overview of how CH enhances cardiac tolerance to ischemia/reperfusion.It is an in-depth analysis of the published data on the underlying mechanisms,which can lead to future development of the cardioprotective effect of CH.A better understanding of the CH-activated protective signaling pathways may contribute to new therapeutic approaches in an increase of cardiac tolerance to ischemia/reperfusion.
文摘Primary coronary revascularization by means of percutaneous coronary intervention(PCI)is a highly effective treatment of acute myocardial infarction re-establishing coronary perfusion and stopping the ongoing necrosis in the dependent myocardium.Single-photon emission computed tomography(SPECT)is the most widely used modality assessing myocardial salvage as the difference between the acute perfusion defect before intervention and the remaining scar size measured in a second scan several days after the event.SPECT allows quantification of area at risk(AAR)and final infarct size(FIS)by tracer injection prior to revascularization and after 1 month,respectively.SPECT provides the most validated measure of myocardial salvage and has been utilized in multiple randomizedclinical trials.However,SPECT is logistically challenging,expensive,and includes radiation exposure.More recently,a large number of studies have suggested that cardiac magnetic resonance(CMR)can determine salvage in a single examination by combining measures of myocardial oedema in the AAR exposed to ischaemia reperfusion with FIS quantification by late gadolinium enhancement.
