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

Abstract

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.

Figure 1

Perfused mouse brain three hours after experimental SAH (endovascular perforation model). A large clot formed at the perforation site (dotted white circle), and blood is distributed from the bleeding site into the subarachnoid space, preferentially along blood vessels.

Figure 2

Intracranial pressure (ICP; (a)), mean arterial blood pressure (MAP; (b)) and cerebral perfusion pressure (CPP; (c)) after SAH in a mouse (t = 0; endovascular perforation model).