Subarachnoid hemorrhage and transient global cerebral ischemia result in similar pathophysiological changes in the cerebral microcirculation. These changes include microvascular constriction, increased leukocyte-endothelial interactions, blood brain barrier disruption, and microthrombus formation. This paper will look at various animal and preclinical studies that investigate these various microvascular changes, perhaps providing insight in how these microvessels can be a therapeutic target in both subarachnoid hemorrhage and transient global cerebral ischemia. 1. Introduction Subarachnoid hemorrhage (SAH) is a type of hemorrhagic stroke, most commonly caused by a ruptured intracranial aneurysm. At the time of aneurysm rupture, blood pours into the subarachnoid space, and the intracranial pressure (ICP) inside the rigid calvarium increases sharply, causing a corresponding decrease in cerebral blood flow (CBF). The patient’s clinical presentation on arrival to the hospital can depend on the degree and duration of this initial global cerebral ischemia. Patients with aneurysmal SAH may develop angiographic vasospasm and delayed cerebral ischemia (DCI) with onset 3–12 days after the initial rupture [1]. DCI may or may not be accompanied by large artery vasospasm as seen with vascular imaging [2]. A multicenter randomized clinical trial has not shown improvement in neurologic outcome despite ameliorating the delayed large artery vasospasm [3]. Whether this is due to efficacy of rescue therapy in the placebo groups or drug toxicity abrogating beneficial effects in the clazosentan groups has not been resolved. Nevertheless, as a result of these results, research in SAH has also investigated early brain injury and acute microvascular changes [4]. Nimodipine, an L-type calcium channel antagonist, is the only pharmacologic agent that has been shown to consistently improve neurologic outcomes in clinical trials of patients with SAH [5]. Similarly, cardiac arrest (CA) results in global cerebral ischemia that is transient in clinically relevant cases, since if cardiac function is not restored, the situation is of pathological interest only. Other causes of transient global cerebral ischemia (tGCI) include asphyxia, shock, and complex cardiac surgery [6]. The clinical presentation depends on the duration of cardiac arrest and time to initiating cardiopulmonary resuscitation. After global cerebral ischemia from SAH or tGCI, a cascade of molecular events occurs, resulting in variable degrees of brain injury and cerebrovascular changes. Global cerebral ischemia in
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