A Pathological Study of Cerebrovascular Diseases in Spontaneously Hypertensive Rats

Abstract

Brains of spontaneously hypertensive rats (SHR) were histopathogically studied, and the effects of salt loading on the cerebrovascular diseases were investigated. Brains of SHR showed hemorrhage, necrosis and edema. As the morphological cause of hemorrhage, microaneurysms were observed in the hemorrhagic foci. Cellular hyperplasia of the pial arteries, hyaline degeneration, fibrinoid necrosis and thrombus formation of the intracerebral arterioles and small arteries were found as the cause of necrosis of the brains. In the study of vascular permeability using horse-radish peroxidase as a marker, an increased vascular permeability was demonstrated in the rats with very high blood pressure beyond 220 mmHg. For the development of fibrinoid necrosis, thrombus formation and an increased vascular permeability, endothelial injury due to hypertension seems to play an important role. Because the localization of increased cerebrovascular permeability corresponded well with that of cerebral necrosis, and there were transitional findings between brain edema and cyst formation in the brain, at least some necrotic foci were suggested to be caused by an increased cerebrovascular permeability. The incidence of cerebrovascular changes was high in stroke-prone substrains such as A 1-sb and A3. The effects of promoting hypertension by salt loading were especially severe in the above substrains.