scholarly journals Pathophysiological Role of Global Cerebral Ischemia following Subarachnoid Hemorrhage: The Current Experimental Evidence

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Nikolaus Plesnila
Keyword(s):  
Cardiac Arrest ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Mortality Rates ◽  
Experimental Models ◽  
Global Cerebral Ischemia ◽  
Pathophysiological Role

Subarachnoid hemorrhage (SAH) is the subtype of stroke with one of the highest mortality rates and the least well-understood pathophysiologies. One of the very early events which may occur after SAH is a significant decrease of cerebral perfusion pressure (CPP) caused by the excessive increase of intracranial pressure during the initial bleeding. A severely decreased CPP results in global cerebral ischemia, an event also occurring after cardiac arrest. The aim of the current paper is to review the pathophysiological events occurring in experimental models of SAH and global cerebral ischemia and to evaluate the contribution and the importance of global cerebral ischemia for the pathophysiology of SAH.

scholarly journals Adenosine A2A receptors in early ischemic vascular injury after subarachnoid hemorrhage

2010 ◽  
Vol 113 (4) ◽  
pp. 826-834 ◽  
Author(s):  
Fatima A. Sehba ◽  
Rowena Flores ◽  
Artur Muller ◽  
Victor Friedrich ◽  
Jiang-Fan Chen ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Knockout Mice ◽  
Cerebral Perfusion ◽  
Type Iv Collagen ◽  
Perfusion Pressure ◽  
Internal Diameter ◽  
Vascular Response ◽  
Wild Type ◽  
Type Iv

Object The role of adenosine A2A receptors in the early vascular response after subarachnoid hemorrhage (SAH) is unknown. In other forms of cerebral ischemia both activation and inhibition of A2A receptors is reported to be beneficial. However, these studies mainly used pharmacological receptor modulation, and most of the agents available exhibit low specificity. The authors used adenosine A2A receptor knockout mice to study the role of A2A receptors in the early vascular response to SAH. Methods Subarachnoid hemorrhage was induced in wild-type mice (C57BL/6) and A2A receptor knockout mice by endovascular puncture. Cerebral blood flow, intracranial pressure, and blood pressure were recorded, and cerebral perfusion pressure was deduced. Animals were sacrificed at 1, 3, or 6 hours after SAH or sham surgery. Coronal brain sections were immunostained for Type IV collagen, the major protein of the basal lamina. The internal diameter of major cerebral arteries and the area fraction of Type IV collagen–positive microvessels (< 100 μm) were determined. Results The initial increase in intracranial pressure and decrease in cerebral perfusion pressure at SAH induction was similar in both types of mice, but cerebral blood flow decline was significantly smaller in A2A receptor knockout mice as compared with wild-type cohorts. The internal diameter of major cerebral vessels decreased progressively after SAH. The extent of diameter reduction was significantly less in A2A receptor knockout mice than in wild-type mice. Type IV collagen immunostaining decreased progressively after SAH. This decrease was significantly less in A2A receptor knockout mice than in wild-type mice. Conclusions These results demonstrate that global inactivation of A2A receptors decreases the intensity of the early vascular response to SAH. Early inhibition of A2A receptors after SAH might reduce cerebral injury.

scholarly journals Role of Endothelin-1 in Human Aneurysmal Subarachnoid Hemorrhage: Associations with Vasospasm and Delayed Cerebral Ischemia

2011 ◽  
Vol 15 (1) ◽  
pp. 19-27 ◽  
Author(s):  
Bhavani P. Thampatty ◽  
Paula R. Sherwood ◽  
Matthew J. Gallek ◽  
Elizabeth A. Crago ◽  
Dianxu Ren ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Endothelin 1

Improved Resuscitation after Cardiac Arrest in Rats Expressing the Baculovirus Caspase Inhibitor Protein p35 in Central Neurons

2003 ◽  
Vol 99 (1) ◽  
pp. 112-121 ◽  
Author(s):  
Peter Vogel ◽  
Herman v.d. Putten ◽  
Erik Popp ◽  
Jakub J. Krumnikl ◽  
Peter Teschendorf ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Cerebral Ischemia ◽  
Neuronal Death ◽  
Neurologic Deficit ◽  
Global Cerebral Ischemia ◽  
Cardiac Massage ◽  
Caspase Inhibitor ◽  
Central Neurons ◽  
Cornu Ammonis ◽  
Baculovirus P35

Background Global cerebral ischemia is associated with delayed neuronal death. Given the role of caspases in apoptosis, caspase inhibitors may provide neuronal protection after cardiac arrest. To this end, the authors generated a transgenic rat line expressing baculovirus p35, a broad-spectrum caspase inhibitor, in central neurons. Its effects were evaluated on neuronal cell death and outcome after global cerebral ischemia. Methods Global cerebral ischemia was induced by cardiocirculatory arrest. After 6 min, animals were resuscitated by controlled ventilation, extrathoracic cardiac massage, epinephrine, and electrical countershocks. Neuronal death was assessed after 7 days by histologic evaluation of the hippocampal cornu ammonis 1 sector. Postischemic outcome was assessed by determination of overall survival and according to neurologic deficit scores 24 h, 3 days, and 7 days after resuscitation. Results The rate of 7-day survival after cardiac arrest for the transgenic rats (85%) was significantly higher than that for the nontransgenic controls (52%; P &lt; 0.05). However, no differences were observed either in the number of terminal deoxynucleotidyltransferase-mediated d-uracil triphosphate-biotin nick end-labeling-positive cells or viable neurons in the cornu ammonis 1 sector or in the neurologic deficit score when comparing surviving transgenic and nontransgenic rats. These findings suggest that neuronal apoptosis after cardiac arrest is not primarily initiated by activation of caspases. Conclusion Expression of baculovirus p35 can improve survival after cardiac arrest in rats, but the mode and site of action remain to be elucidated.

scholarly journals Role of Protease-Activated Receptor-1 in Brain Injury After Experimental Global Cerebral Ischemia

Stroke ◽  
2012 ◽  
Vol 43 (9) ◽  
pp. 2476-2482 ◽  
Author(s):  
Jinhu Wang ◽  
Hang Jin ◽  
Ya Hua ◽  
Richard F. Keep ◽  
Guohua Xi
Keyword(s):  
Brain Injury ◽  
Cerebral Ischemia ◽  
Global Cerebral Ischemia ◽  
Protease Activated Receptor 1
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