Contribution of Platelet Aggregation and Serotonin Release to Progressive Cerebral Infarction

Abstract

Prevention and amelioration of acute cerebral infarction resulting from occlusion of the aortocerebral arterial circulation is best effected by maintenance of tissue metabolic viability by enhancing the cerebral collateral circulation. This may be achieved by several therapeutic approaches but let us consider here the role of components of the blood in the ischemic zone, particularly the platelet. Certain conditions contribute to impairment of the cerebral collateral circulation and hence are responsible for the diminished perfusion so commonly found after ischemia when occlusion of major cerebral vessels is relieved, which has sometimes been termed the “no reflow” phenomenon (Ames et al., 1968). Conditions contributing to “no reflow” include intraluminal aggregation of blood elements, swelling of perivascular astrocytes due to edema formation with vascular compression and vasospasm (Meyer, 1961) (Fig. 1). This paper examines in detail the possible participation of the platelet in such adverse pathophysiologic conditions that may contribute to progression of cerebral infarction.

This work was supported by Grant NS 09287 from the National Institute of Neurological Diseases and Stroke, and in part by Grant RR 00350 from the General Clinical Research Centers Branch, Division of Research Resources, National Institutes of Health, Bethesda, Maryland 20014

James Buckingham was awarded a Student Clerkship from the American Heart Association, Stroke Council