Cerebral circulation and the initiation mechanism of stroke in stroke-prone spontaneously hypertensive rats (SHRSP).

Abstract

The predilection sites of cerebrovascular lesions (cerebral hemorrhage and/or softening) were studied in 1, 278 SHRSP. The precise supply to the main cerebral arteries was determined by trypan blue injections and microangiography. The three major territories were the anteromedial cortex, the occipital cortex, and the basal ganglia. A common angioarchitectural characteristic of these areas was the blood supply throughrecurrent branchinfrom the main stream. In the basal ganglia, where there is a preponderance of lesions, the arteries responsible for these lesions belonged to the lateral group of lenticulostriate arteries. The primary prestroke arterial lesions were further studied microangiographically in SHRSP killed at the time the initial symptoms of stroke were detected. These points were located at theboundary zoneof the main cerebral arteries. Such findings indicated the importance of these two angioarchitectural minor loci as the basis for functional or organic circulatory disturbances that might cause stroke. Since these local factors for fufactors for stroke are common in the cortex and basal ganglia of rats and basal ganglia of humans, these SHRSP are regarded as good pathogenetic models for studies on stroke in humans. After simultaneous bilateral carotid ligation, accelerated induction of cerebrovascular lesons in young SHRSP and stroke-resistant SHR (SHRSR) showed predilection sites of stroke approximately consistent with those in SHRSP after natural death. (and rather consistent with those in humans). Such findings comfirmed that these lesions developed at theminor lociof cerebral circulation fed byrecurrent branchesfrom the main cerebral arteries. Regional cerebral blood flow (rCBF) was repeatedly measured by the hydrogen clearance method in both frontal and temporal cortices of SHRSP at the age of 50 days and thereafter. When SHRSP developed severe hypertension over 200 mmHg at the age of 60 days, rCBF in both frontal and temporal cortices began to decrease abruptly, especially in the frontal region of the cortex-one of the three pretension and at the hypertensive steady state, the frontal region constantly showed lower rCBF values than the temporal region. In contrast, such a reduction in rCBF was not noted in either SHRSR which developed moderate hypertension under 200 mmHg, or in Wistar-Kyoto rats (WK) with normal blood pressure under 150 mmHg.