Influence of Systemic Blood Pressure on Blood Flow and Microcirculation of Ischemic Cerebral Cortex: a Failure of Autoregulation

Abstract

Publisher Summary Cortical pallor, either focal or generalized, was the earliest definite sign of cortical ischemia. Once pallor was established, spontaneous recolorization of the cortex rarely occurred. Constriction or “spasm” of superficial cortical arteries and arterioles frequently accompanied ischemia. Ischemic changes occurring in the superficial cortical microvasculature and microcirculation after occlusion of the ipsilateral middle cerebral artery probably were representative of the process of cerebral infarction. In the studies made, ischemic changes occurred regularly after arterial occlusion, even though systemic blood pressure remained at normotensive levels. Systemic hypotension, spontaneous or produced by drugs or the removal of blood, speeds the development and increases the severity of ischemic changes in the microcirculation, but does not alter the character of such changes. Hypotension after arterial occlusion results in a further reduction of cortical blood flow which appears to be passive, indicating a failure of autoregulation of flow. Autoregulation may fail because of tissue damage or because there is a maximal response to ischemia. Systemic hypertension, spontaneous or produced by drugs, does not influence ischemic changes in the microcirculation, except for the fact that when platelet thrombi are present in veins, venous hemorrhage often occurs. An increase in systemic blood pressure does not produce an increase in blood flow through the ischemic cortex, except when hypotension previously has been present. In the latter instance, blood in veins may become redder, also indicating a failure of autoregulation of cortical blood flow.