Further Studies on the Mechanisms of Stroke in Stroke-Prone SHRDecrease in Regional Cerebral Blood Flow and Catecholamine Depletion

摘要

Chronic rCBF reduction under severe hypertensive state preceded the development of vascular damages in SHRSP, and by controlling blood pressure under 200mmHg rCBF was maintained well within normal range so that no stroke was observed. Noradrenaline fluorescence was reduced in cerebral lesions which developed spontaneously in SHRSP. When rCBF was reduced in young SHRSP acutely after the bilateral ligation of carotid arteries, depletion of noradrenaline and dopamine was noted. From this observation catecholamines seem to be released when nerve terminals are exposed to hypoxia. It may be possible that released catecholamines accelerate the vasoconstriction of cerebral arteries and further decrease the blood supply to the areas, thus to increase vascular permeability which results in arterionecrosis and/or thrombus formation. Thus, catecholamines might be involved in the vicious circle for inducing cerebrovascular lesions.