Following subarachnoid hemorrhage, vasoconstrictor substances, cellular apoptosis, blood coagulation, and vascular cell proliferation affect the onset of cerebral vasospasm. Previous studies from our laboratory have r...Following subarachnoid hemorrhage, vasoconstrictor substances, cellular apoptosis, blood coagulation, and vascular cell proliferation affect the onset of cerebral vasospasm. Previous studies from our laboratory have revealed that injection of lidocaine （2 mg） into the cisterna magna reduces cerebral vasospasm and nerve functional impairment in an animal model of subarachnoid hemorrhage. The present study determined the optimal lidocaine dose for vasospasm and brain injury by injecting different doses of lidocaine into the cisterna magna in a rabbit model of subarachnoid hemorrhage. Results showed that endothelin, tumor necrosis factor-a, and interleukin-6 levels significantly increased in plasma, and calcitonin gene-related peptide levels significantly decreased in plasma （P 〈 0.05）. The number of neurons was decreased, the number of cells expressing c-Fos increased in the hippocampus, and cross-sections and diameters of basilar arteries were reduced （P 〈 0.05）. These changes significantly improved following injection of lidocaine （1,2, 4, and 6 mg） into the cisterna magna. A dose of 6 mg lidocaine into the cisterna magna resulted in optimal effects on cerebral vasospasm and brain injury following subarachnoid hemorrhage.展开更多
Objective.To investigate the effects of Ginkgo biloba extracton cer ebral vasospasmafter subarachnoid hemorrhageand its influence on n itric oxideand endothelin-l .Methods.Noncraniotomy models of SAH in Wistar rats we...Objective.To investigate the effects of Ginkgo biloba extracton cer ebral vasospasmafter subarachnoid hemorrhageand its influence on n itric oxideand endothelin-l .Methods.Noncraniotomy models of SAH in Wistar rats were used and animals were divided into sham-operated group ,SAH group,saline-treated group and EGb-treated group.Diameter of basilar a rtery was measured.Regional cerebral blood flow,NO and ET-1levels in blood,and calcium content in brain tissue within24hours after SAH were dete cted.Pathological examination of hippocampus CA1sub-field was also performed .Results.Sham operation did not alter the above parameters.Induction of SAH l ed to a marked spasm of basilar artery.rCBF decreased obviously and consecutive ly within24hours after SAH.Meanwhile NO level in serum decreased,ET-1level in plasma and calcium content in brain tissue significantly in-creased.Pyra midal cells in hippocampus CA1subfield were severely damaged.EGb significantly antago-nized the pathological alterations of the above parameters.Conclusion .Alterations of NO,and ET-1play an important role in the development of CV S after SAH.EGb exerts its protective effects on CVS by inhibitng the above pat hological alterations.展开更多
In this manuscript a comprehensive coverage of recent developments in the drug therapy of vasospasm while providing the background information that neuroscientists need to understand its rationale. The range of new ag...In this manuscript a comprehensive coverage of recent developments in the drug therapy of vasospasm while providing the background information that neuroscientists need to understand its rationale. The range of new agents available for treatment of cerebral vasospasm is expanding rapidly along with rapid advances in pharmacology and physiology that are uncovering the mechanisms of this disease. Although there are many publications for treatment of cerebral vaso-spasm, most are focusing on different aspects of vasospasm treatment and many have limited value due to insufficient quality. Moreover, the complexity of this, in many cases deleterious condition, is enormous and the information needed to understand drug effects is accordingly often not readily available in a single source. A number of pharmacological and medical therapies are currently in use or being investigated in an attempt to reverse cerebral vasospasm, but only a few have proven to be useful. Current research efforts promise the eventual production of new medical therapies. At last, recommendations for the use of different treatment stages based on currently available clinical data are provided.展开更多
<strong>Objective:</strong> To investigate the therapeutic effect of Shenmai Injection on postoperative cerebral vasospasm in patients with ruptured aneurysms. <strong>Methods:</strong> Seventy...<strong>Objective:</strong> To investigate the therapeutic effect of Shenmai Injection on postoperative cerebral vasospasm in patients with ruptured aneurysms. <strong>Methods:</strong> Seventy patients undergoing craniotomy for ruptured aneurysms in our hospital were selected as study subjects and randomly divided into control (n = 33) and research (n = 37) groups, they were treated with nimodipine and nimodipine combined with Shenmai injection after operation. The blood flow velocity in the middle cerebral artery (MCA) before and at 1, 3, 7, 11 and 14 days after surgery and the incidence of cerebral vasospasm during these days were compared, and the GCS scores at 14 days postoperatively and GOS scores at 6 months postoperatively were compared between the two groups.<strong> Results:</strong> There were no statistically significant differences in the occurrence of cerebral vasospasm, GCS or GOS scores between the two groups (<em>P</em> > 0.05), but the period of postoperative cerebral vasospasm in the study group was significantly shorter than that in the control group. <strong>Conclusion:</strong> Shenmai injection has the effect of shortening the cycle of occurrence of cerebral vasospasm after the operation of ruptured aneurysms, promoting patients to recover as early as possible and reducing their physical and mental burden.展开更多
Laser-Doppler flowmetry was employed in the observation of regional cortical blood flow (rCBF) after experimental subarachnoid hemorrhage (SAH) in anesthetized rats and the contents of endothelin (ET) in the cerebral-...Laser-Doppler flowmetry was employed in the observation of regional cortical blood flow (rCBF) after experimental subarachnoid hemorrhage (SAH) in anesthetized rats and the contents of endothelin (ET) in the cerebral-spinal fluid (CSF), plasma, hypothalamus, cerebral cortex, cerebellum and medulla were simultaneously measured. There was a biphasic change of rCBF after SAH. The contents of ET in CSF, plasma and hypothalamus rose prominently in the early stage after SAH, and the ET-increase in CSF and hypothalamus was earlier than that in plasma. The changes of ET contents in CSF correlated well with that in hypothalamus. Our results suggest that ET probably is an early important factor which induces cerebral vasospasm (CVS) after SAH. The increase of ET in CSF, which may originate from the hypothalamus, might play a more important role in the development of CVS after SAH than that in plasma.展开更多
Cerebral vasospasm (CVS) is a common and severe complication of aneurysmal subarachnoid hemorrhage (aSAH). Despite the improvement in treatment of aSAH, CVS complicating aSAH has remained the main cause of death. CVS ...Cerebral vasospasm (CVS) is a common and severe complication of aneurysmal subarachnoid hemorrhage (aSAH). Despite the improvement in treatment of aSAH, CVS complicating aSAH has remained the main cause of death. CVS begins most often on the third day after the ictal event and reaches the maximum on the 5th–7th postictal days. Several therapeutic modalities have been employed to prevent or reverse CVS. The aim of this review is to summate all the available drug treatment modalities for vasospasm.展开更多
Background: Aneurysmal subarachnoid hemorrhage (aSAH) is an acute neurosurgical emergency with a significant fatality rate. In addition to acute brain injury, a considerable part of patients suffering from aSAH develo...Background: Aneurysmal subarachnoid hemorrhage (aSAH) is an acute neurosurgical emergency with a significant fatality rate. In addition to acute brain injury, a considerable part of patients suffering from aSAH develops secondary brain damage such as cerebral vasospasm (CVS). CVS exacerbates the mortality. Therefore, it is urgently needed to find a biomarker, which could predict secondary brain and lead to operation by physicians more promptly. S100B, produced and released by astrocytes, has proven to be an important biomarker for brain injury.Methods: In this present study, 51 patients with aSAH were included. Five CSF samples from each patient were obtained via lumbar puncture and were detected using electrochemiluminescence immunoassay (ECLIA).Results: It indicated that S100B had a higher concentration in CSF of patients treated by surgical clipping after aSAH than that treated with endovascular coiling. In addition, the mean CSF S100B level in patients without CVS was much lower compared with patients with CVS. And, the expression of S100B increased along with the Fisher Grade at the same day after aSAH attacked and decreased as time went on. Moreover, the CSF S100B level of different time points and the mean CSF S100B level can predict the risk of CVS.Conclusions: These data suggest that CSF S100B can be served as a predictor of CVS, which triggers an immediate management by clinicians to prevent secondary exacerbation.展开更多
Background:Cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH) is a serious and significant health problem in the worldwide.There are still no effective therapies for treatment of CVS in patients suffering fr...Background:Cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH) is a serious and significant health problem in the worldwide.There are still no effective therapies for treatment of CVS in patients suffering from SAH.Our early studies have demonstrated that the expression of connexin43 (Cx43,a member of gap junctional proteins) in cerebral spastic vessel is significantly up-regulated,and knocking down Cx43 with specific siRNA interference can significantly alleviate CVS after SAH.Therefore,Cx43 in cerebral vessel is a potential target in the treatment of CVS.However,Cx43 is widely distributed in many organs,particularly in the heart,and plays an important role in the physiological function.This study is aimed at identify whether OPN,TNC or E-selectin can be used as a target protein to be recognized in spastic cerebral vessels,then we can produce a carrier containing Cx43 siRNA or other inhibitors as a new potential treatment for CVS.Methods:Twenty eight male Sprague Dawley rats (weighing 300-350 g) were randomly divided into either SAH (n =16) or sham group (n =12).The double hemorrhage model was performed on day 0 and 1.All animals were sacrificed after performing India ink angiography on day 5.Initially,the expression of E-selectin,TNC and OPN in cerebral arteries,thoracic aorta and abdominal aorta were analyzed respectively by immunohistochemical staining,western blot in both groups.Then,only those with less expression in thoracic aorta,abdominal aorta and normal cerebral arteries,but higher expression in cerebral spastic arteries were further detected in the spinal cord,heart,kidney,liver,spleen,lung,pancreas,mesenteric and pulmonary arteries,retina and brain tissue,respectively.Results:TNC,OPN and E-selectin were markedly elevated in the spastic cerebral arteries in SAH group but not in control group.The expression of TNC,but not OPN and E-selectin,is abundant in both groups of thoracic aorta and abdominal aorta.Further study demonstrated that expression of OPN,but not E-selecting,in both groups is relatively rich in brain tissue,kidney,pancreas,mesenteric artery,spinal cord and retina,but in heart,liver,lung and pulmonary artery.However,the positive expression of E-selectin was detected in spleen in both groups.Conclusions:TNC is highly expressed in thoracic aorta and abdominal aorta,so it is unsuitable for being a recognition protein.Although OPN,unlike TNC,does not express much in vascular system,but it expresses in many other organs or tissues.However,E-selecting could be considered as a potential recognition protein because it is not so widely distributed in the organs or tissues detected.展开更多
BACKGROUND Coronary artery vasospasm(CAV)is a reversible,transient form of vasoconstriction with clinical manifestations ranging from stable angina to acute coronary syndromes(ACS).Vasospasm of epicardial coronary art...BACKGROUND Coronary artery vasospasm(CAV)is a reversible,transient form of vasoconstriction with clinical manifestations ranging from stable angina to acute coronary syndromes(ACS).Vasospasm of epicardial coronary arteries or associated micro-vasculature can lead to total or subtotal occlusion and has been demonstrated in nearly 50%of patients undergoing angiography for suspected ACS.The mechanism for CAV has been described in literature,but in a subgroup of patients presenting with intracranial hemorrhage,it appears to be multifactorial.These patients tend to have electrocardiographic changes,elevation of cardiac biomarkers of injury and neurogenic stress cardiomyopathy.CASE SUMMARY A 44-year-old woman presented with severe headaches and tonic-clonic seizures.She was found to have diffuse subarachnoid hemorrhage(SAH)requiring ventricular drain placement,coil embolization and induced hypertension.She subsequently developed chest pain with ST elevations in anterior precordial leads,elevated cardiac enzymes and apical ballooning with left ventricular ejection fraction of 35%on transthoracic echocardiogram.Coronary angiogram revealed severe diffuse triple vessel stenoses secondary to CAV seen distally.Subsequent cardiac MRI notable for apical non-viability and scar formation.CONCLUSION This case highlights a unique etiology of acute myocardial infarction in a patient with SAH leading to ST elevations,diffuse triple vessel CAV and apical scar.展开更多
Neuroinflammation is a well-recognized consequence of subarachnoid hemorrhage（SAH）, and Toll-like receptor（TLR） 4 may be an important therapeutic target for post-SAH neuroinflammation. Of the TLR family members, T...Neuroinflammation is a well-recognized consequence of subarachnoid hemorrhage（SAH）, and Toll-like receptor（TLR） 4 may be an important therapeutic target for post-SAH neuroinflammation. Of the TLR family members, TLR4 is expressed in various cell types in the central nervous system, and is unique in that it can signal through both the myeloid differentiation primary-response protein 88-dependent and the toll receptor associated activator of interferon-dependent cascades to coordinate the maximal inflammatory response. TLR4 can be activated by many endogenous ligands having damage-associated molecular patterns including heme and fibrinogen at the rupture of an intracranial aneurysm, and the resultant inflammatory reaction and thereby tissue damages may furthermore activate TLR4. It is widely accepted that the excreted products of TLR4 signaling alter neuronal functions. Previous studies have focused on the pathway through nuclear factor（NF）-κΒ signaling among TLR4 signaling pathways as to the development of early brain injury（EBI） such as neuronal apoptosis and blood-brain barrier disruption, and cerebral vasospasm. However, many findings suggest that both pathways via NF-κΒ and mitogen-activated protein kinases may be involved in EBI and cerebral vasospasm development. To overcome EBI and cerebral vasospasm is important to improve outcomes after SAH, because both EBI and vasopasm are responsible for delayed brain injuries or delayed cerebral ischemia, the most important preventable cause of poor outcomes after SAH. Increasing evidence has shown that TLR4 signaling plays an important role in SAH-induced brain injuries. Better understanding of the roles of TLR4 signaling in SAH will facilitate development of new treatments.展开更多
Numerous studies have demonstrated that endothelin-1 combines with endothelin receptor A, resulting in intense vasoconstriction. Although calcitonin gene-related peptide （CGRP） suppresses endothelin-1, CGRP and endo...Numerous studies have demonstrated that endothelin-1 combines with endothelin receptor A, resulting in intense vasoconstriction. Although calcitonin gene-related peptide （CGRP） suppresses endothelin-1, CGRP and endothelin receptor A exhibit direct biological effects on brain tissue. The present study analyzed CGRP and endothelin receptor A expression following subarachnoid hemorrhage in rabbits using immunohistochemistry. CGRP expression was significant at 5 days after model establishment, and endothelin receptor A expression was significant at 3 days after model induction. The perimeter of the basilar artery was measured to determine the amount of cerebral vasospasm. Analytical results revealed a significantly shortened basilar artery perimeter following subarachnoid hemorrhage. Changes in the basilar artery perimeter were negatively associated with endothelin receptor A expression, but positively correlated with CGRP expression in vessels. These results suggest that following subarachnoid hemorrhage, CGRP and endothelin receptor A expressions dynamically changed in brain vessels and tissues, although these changes were not synchronous. Changes in endothelin receptor A expression exhibited a significant effect on the occurrence and development of delayed cerebral vasospasm and delayed neuronal death, while CGRP relaxed vessels and protected nerves.展开更多
Objective: To investigate the role of endothelin 1 (ET 1) in development of ischemic brain damage after subarachnoid hemorrhage (SAH), and the protective effect of Ginkgo biloba extract (GBE) on it. Methods: Noncr...Objective: To investigate the role of endothelin 1 (ET 1) in development of ischemic brain damage after subarachnoid hemorrhage (SAH), and the protective effect of Ginkgo biloba extract (GBE) on it. Methods: Noncraniotomy SAH models of Wistar rat were divided into SAH group and GBE treated group, the diameter of basilar artery (BA), dynamic changes of regional cerebral blood flow (rCBF) and ET 1 content of intracranial plasma within 24 hours after SAH of both groups were determined. And pathological examination of CA1 region of hippocampus was performed 3 days later. Results: rCBF decreased and ET 1 content increased obviously and steadily in 24 hours after SAH. Spasm of BA occurred half an hour after SAH and neurons of hippocampus CA1 region were damaged severely. GBE could antagonize the above mentioned pathological changes effectively. Conclusion:Increase of ET 1 is an important factor leading to ischemic brain damage after SAH. GBE exerts its protective effect by antagonizing pathological increase of ET 1.展开更多
基金the Science and Technology Foundation of Guizhou Province, No. J20072118
文摘Following subarachnoid hemorrhage, vasoconstrictor substances, cellular apoptosis, blood coagulation, and vascular cell proliferation affect the onset of cerebral vasospasm. Previous studies from our laboratory have revealed that injection of lidocaine （2 mg） into the cisterna magna reduces cerebral vasospasm and nerve functional impairment in an animal model of subarachnoid hemorrhage. The present study determined the optimal lidocaine dose for vasospasm and brain injury by injecting different doses of lidocaine into the cisterna magna in a rabbit model of subarachnoid hemorrhage. Results showed that endothelin, tumor necrosis factor-a, and interleukin-6 levels significantly increased in plasma, and calcitonin gene-related peptide levels significantly decreased in plasma （P 〈 0.05）. The number of neurons was decreased, the number of cells expressing c-Fos increased in the hippocampus, and cross-sections and diameters of basilar arteries were reduced （P 〈 0.05）. These changes significantly improved following injection of lidocaine （1,2, 4, and 6 mg） into the cisterna magna. A dose of 6 mg lidocaine into the cisterna magna resulted in optimal effects on cerebral vasospasm and brain injury following subarachnoid hemorrhage.
文摘Objective.To investigate the effects of Ginkgo biloba extracton cer ebral vasospasmafter subarachnoid hemorrhageand its influence on n itric oxideand endothelin-l .Methods.Noncraniotomy models of SAH in Wistar rats were used and animals were divided into sham-operated group ,SAH group,saline-treated group and EGb-treated group.Diameter of basilar a rtery was measured.Regional cerebral blood flow,NO and ET-1levels in blood,and calcium content in brain tissue within24hours after SAH were dete cted.Pathological examination of hippocampus CA1sub-field was also performed .Results.Sham operation did not alter the above parameters.Induction of SAH l ed to a marked spasm of basilar artery.rCBF decreased obviously and consecutive ly within24hours after SAH.Meanwhile NO level in serum decreased,ET-1level in plasma and calcium content in brain tissue significantly in-creased.Pyra midal cells in hippocampus CA1subfield were severely damaged.EGb significantly antago-nized the pathological alterations of the above parameters.Conclusion .Alterations of NO,and ET-1play an important role in the development of CV S after SAH.EGb exerts its protective effects on CVS by inhibitng the above pat hological alterations.
文摘In this manuscript a comprehensive coverage of recent developments in the drug therapy of vasospasm while providing the background information that neuroscientists need to understand its rationale. The range of new agents available for treatment of cerebral vasospasm is expanding rapidly along with rapid advances in pharmacology and physiology that are uncovering the mechanisms of this disease. Although there are many publications for treatment of cerebral vaso-spasm, most are focusing on different aspects of vasospasm treatment and many have limited value due to insufficient quality. Moreover, the complexity of this, in many cases deleterious condition, is enormous and the information needed to understand drug effects is accordingly often not readily available in a single source. A number of pharmacological and medical therapies are currently in use or being investigated in an attempt to reverse cerebral vasospasm, but only a few have proven to be useful. Current research efforts promise the eventual production of new medical therapies. At last, recommendations for the use of different treatment stages based on currently available clinical data are provided.
文摘<strong>Objective:</strong> To investigate the therapeutic effect of Shenmai Injection on postoperative cerebral vasospasm in patients with ruptured aneurysms. <strong>Methods:</strong> Seventy patients undergoing craniotomy for ruptured aneurysms in our hospital were selected as study subjects and randomly divided into control (n = 33) and research (n = 37) groups, they were treated with nimodipine and nimodipine combined with Shenmai injection after operation. The blood flow velocity in the middle cerebral artery (MCA) before and at 1, 3, 7, 11 and 14 days after surgery and the incidence of cerebral vasospasm during these days were compared, and the GCS scores at 14 days postoperatively and GOS scores at 6 months postoperatively were compared between the two groups.<strong> Results:</strong> There were no statistically significant differences in the occurrence of cerebral vasospasm, GCS or GOS scores between the two groups (<em>P</em> > 0.05), but the period of postoperative cerebral vasospasm in the study group was significantly shorter than that in the control group. <strong>Conclusion:</strong> Shenmai injection has the effect of shortening the cycle of occurrence of cerebral vasospasm after the operation of ruptured aneurysms, promoting patients to recover as early as possible and reducing their physical and mental burden.
文摘Laser-Doppler flowmetry was employed in the observation of regional cortical blood flow (rCBF) after experimental subarachnoid hemorrhage (SAH) in anesthetized rats and the contents of endothelin (ET) in the cerebral-spinal fluid (CSF), plasma, hypothalamus, cerebral cortex, cerebellum and medulla were simultaneously measured. There was a biphasic change of rCBF after SAH. The contents of ET in CSF, plasma and hypothalamus rose prominently in the early stage after SAH, and the ET-increase in CSF and hypothalamus was earlier than that in plasma. The changes of ET contents in CSF correlated well with that in hypothalamus. Our results suggest that ET probably is an early important factor which induces cerebral vasospasm (CVS) after SAH. The increase of ET in CSF, which may originate from the hypothalamus, might play a more important role in the development of CVS after SAH than that in plasma.
文摘Cerebral vasospasm (CVS) is a common and severe complication of aneurysmal subarachnoid hemorrhage (aSAH). Despite the improvement in treatment of aSAH, CVS complicating aSAH has remained the main cause of death. CVS begins most often on the third day after the ictal event and reaches the maximum on the 5th–7th postictal days. Several therapeutic modalities have been employed to prevent or reverse CVS. The aim of this review is to summate all the available drug treatment modalities for vasospasm.
文摘Background: Aneurysmal subarachnoid hemorrhage (aSAH) is an acute neurosurgical emergency with a significant fatality rate. In addition to acute brain injury, a considerable part of patients suffering from aSAH develops secondary brain damage such as cerebral vasospasm (CVS). CVS exacerbates the mortality. Therefore, it is urgently needed to find a biomarker, which could predict secondary brain and lead to operation by physicians more promptly. S100B, produced and released by astrocytes, has proven to be an important biomarker for brain injury.Methods: In this present study, 51 patients with aSAH were included. Five CSF samples from each patient were obtained via lumbar puncture and were detected using electrochemiluminescence immunoassay (ECLIA).Results: It indicated that S100B had a higher concentration in CSF of patients treated by surgical clipping after aSAH than that treated with endovascular coiling. In addition, the mean CSF S100B level in patients without CVS was much lower compared with patients with CVS. And, the expression of S100B increased along with the Fisher Grade at the same day after aSAH attacked and decreased as time went on. Moreover, the CSF S100B level of different time points and the mean CSF S100B level can predict the risk of CVS.Conclusions: These data suggest that CSF S100B can be served as a predictor of CVS, which triggers an immediate management by clinicians to prevent secondary exacerbation.
文摘Background:Cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH) is a serious and significant health problem in the worldwide.There are still no effective therapies for treatment of CVS in patients suffering from SAH.Our early studies have demonstrated that the expression of connexin43 (Cx43,a member of gap junctional proteins) in cerebral spastic vessel is significantly up-regulated,and knocking down Cx43 with specific siRNA interference can significantly alleviate CVS after SAH.Therefore,Cx43 in cerebral vessel is a potential target in the treatment of CVS.However,Cx43 is widely distributed in many organs,particularly in the heart,and plays an important role in the physiological function.This study is aimed at identify whether OPN,TNC or E-selectin can be used as a target protein to be recognized in spastic cerebral vessels,then we can produce a carrier containing Cx43 siRNA or other inhibitors as a new potential treatment for CVS.Methods:Twenty eight male Sprague Dawley rats (weighing 300-350 g) were randomly divided into either SAH (n =16) or sham group (n =12).The double hemorrhage model was performed on day 0 and 1.All animals were sacrificed after performing India ink angiography on day 5.Initially,the expression of E-selectin,TNC and OPN in cerebral arteries,thoracic aorta and abdominal aorta were analyzed respectively by immunohistochemical staining,western blot in both groups.Then,only those with less expression in thoracic aorta,abdominal aorta and normal cerebral arteries,but higher expression in cerebral spastic arteries were further detected in the spinal cord,heart,kidney,liver,spleen,lung,pancreas,mesenteric and pulmonary arteries,retina and brain tissue,respectively.Results:TNC,OPN and E-selectin were markedly elevated in the spastic cerebral arteries in SAH group but not in control group.The expression of TNC,but not OPN and E-selectin,is abundant in both groups of thoracic aorta and abdominal aorta.Further study demonstrated that expression of OPN,but not E-selecting,in both groups is relatively rich in brain tissue,kidney,pancreas,mesenteric artery,spinal cord and retina,but in heart,liver,lung and pulmonary artery.However,the positive expression of E-selectin was detected in spleen in both groups.Conclusions:TNC is highly expressed in thoracic aorta and abdominal aorta,so it is unsuitable for being a recognition protein.Although OPN,unlike TNC,does not express much in vascular system,but it expresses in many other organs or tissues.However,E-selecting could be considered as a potential recognition protein because it is not so widely distributed in the organs or tissues detected.
文摘BACKGROUND Coronary artery vasospasm(CAV)is a reversible,transient form of vasoconstriction with clinical manifestations ranging from stable angina to acute coronary syndromes(ACS).Vasospasm of epicardial coronary arteries or associated micro-vasculature can lead to total or subtotal occlusion and has been demonstrated in nearly 50%of patients undergoing angiography for suspected ACS.The mechanism for CAV has been described in literature,but in a subgroup of patients presenting with intracranial hemorrhage,it appears to be multifactorial.These patients tend to have electrocardiographic changes,elevation of cardiac biomarkers of injury and neurogenic stress cardiomyopathy.CASE SUMMARY A 44-year-old woman presented with severe headaches and tonic-clonic seizures.She was found to have diffuse subarachnoid hemorrhage(SAH)requiring ventricular drain placement,coil embolization and induced hypertension.She subsequently developed chest pain with ST elevations in anterior precordial leads,elevated cardiac enzymes and apical ballooning with left ventricular ejection fraction of 35%on transthoracic echocardiogram.Coronary angiogram revealed severe diffuse triple vessel stenoses secondary to CAV seen distally.Subsequent cardiac MRI notable for apical non-viability and scar formation.CONCLUSION This case highlights a unique etiology of acute myocardial infarction in a patient with SAH leading to ST elevations,diffuse triple vessel CAV and apical scar.
基金supported by a Grant-in-Aid for Scientific Research from Mie Medical Research Foundation to Dr.Suzuki
文摘Neuroinflammation is a well-recognized consequence of subarachnoid hemorrhage（SAH）, and Toll-like receptor（TLR） 4 may be an important therapeutic target for post-SAH neuroinflammation. Of the TLR family members, TLR4 is expressed in various cell types in the central nervous system, and is unique in that it can signal through both the myeloid differentiation primary-response protein 88-dependent and the toll receptor associated activator of interferon-dependent cascades to coordinate the maximal inflammatory response. TLR4 can be activated by many endogenous ligands having damage-associated molecular patterns including heme and fibrinogen at the rupture of an intracranial aneurysm, and the resultant inflammatory reaction and thereby tissue damages may furthermore activate TLR4. It is widely accepted that the excreted products of TLR4 signaling alter neuronal functions. Previous studies have focused on the pathway through nuclear factor（NF）-κΒ signaling among TLR4 signaling pathways as to the development of early brain injury（EBI） such as neuronal apoptosis and blood-brain barrier disruption, and cerebral vasospasm. However, many findings suggest that both pathways via NF-κΒ and mitogen-activated protein kinases may be involved in EBI and cerebral vasospasm development. To overcome EBI and cerebral vasospasm is important to improve outcomes after SAH, because both EBI and vasopasm are responsible for delayed brain injuries or delayed cerebral ischemia, the most important preventable cause of poor outcomes after SAH. Increasing evidence has shown that TLR4 signaling plays an important role in SAH-induced brain injuries. Better understanding of the roles of TLR4 signaling in SAH will facilitate development of new treatments.
基金the National 863 Project of China,No. 2006AA02Z4Z4the National Natural Science Foundation of China,No. 30870844+1 种基金the New Century Excellent Talent Support Project of Ministry of Education,No. NCET-05-0831the "13115" Special Fund for Major Science and Technology Projects of Shaanxi Province,No. 2008ZDKG-66
文摘Numerous studies have demonstrated that endothelin-1 combines with endothelin receptor A, resulting in intense vasoconstriction. Although calcitonin gene-related peptide （CGRP） suppresses endothelin-1, CGRP and endothelin receptor A exhibit direct biological effects on brain tissue. The present study analyzed CGRP and endothelin receptor A expression following subarachnoid hemorrhage in rabbits using immunohistochemistry. CGRP expression was significant at 5 days after model establishment, and endothelin receptor A expression was significant at 3 days after model induction. The perimeter of the basilar artery was measured to determine the amount of cerebral vasospasm. Analytical results revealed a significantly shortened basilar artery perimeter following subarachnoid hemorrhage. Changes in the basilar artery perimeter were negatively associated with endothelin receptor A expression, but positively correlated with CGRP expression in vessels. These results suggest that following subarachnoid hemorrhage, CGRP and endothelin receptor A expressions dynamically changed in brain vessels and tissues, although these changes were not synchronous. Changes in endothelin receptor A expression exhibited a significant effect on the occurrence and development of delayed cerebral vasospasm and delayed neuronal death, while CGRP relaxed vessels and protected nerves.
文摘Objective: To investigate the role of endothelin 1 (ET 1) in development of ischemic brain damage after subarachnoid hemorrhage (SAH), and the protective effect of Ginkgo biloba extract (GBE) on it. Methods: Noncraniotomy SAH models of Wistar rat were divided into SAH group and GBE treated group, the diameter of basilar artery (BA), dynamic changes of regional cerebral blood flow (rCBF) and ET 1 content of intracranial plasma within 24 hours after SAH of both groups were determined. And pathological examination of CA1 region of hippocampus was performed 3 days later. Results: rCBF decreased and ET 1 content increased obviously and steadily in 24 hours after SAH. Spasm of BA occurred half an hour after SAH and neurons of hippocampus CA1 region were damaged severely. GBE could antagonize the above mentioned pathological changes effectively. Conclusion:Increase of ET 1 is an important factor leading to ischemic brain damage after SAH. GBE exerts its protective effect by antagonizing pathological increase of ET 1.
