Pathogenesis of Cerebral Hemorrhages in Experimental Hypertension in Rabbits with Particular Reference to Acute Vascular Lesions (Fibrinoid Necrosis) of Small Arteries and Arterioles

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The effect of salt, high blood pressure and renal factors on the development of acute vascular lesions of small arteries and arterioles and cerebral hemorrhages was studied in rabbits through production of hypertension by means of unilateral or bilateral renal injuries. 1 . Massive cerebral hemorrhages were induced in animals with bilateral renal injuries and these were never induced in animals with one ischemic and the other intact kidneys even during advanced stage of hypertension. 2. Animals died ,due to cerebral hemorrhages usually accompanied with marked high blood pressure during the advanced stage. However, cerebral hemorrhages were induced in animals with blood pressure less than 120 mmHg as well as in those with higher blood pressure during the early stage after renal manipulation. 3. Among acute arterial lesions, the most prominent lesion consisted of the fibrinoid necrosis of small arteries and arterioles with a wide distribution. The vessels of gastro-intestinal tract especially those of stomack were predominantly vulneable. 4. Fibrinoid necrosis of small arteries and arterioles in the brain was found all of the experiments with cerebral hemorrhages. The incidence of the acute arterial lesion in the brain and other tissues was higher in experimental groups in which cerebral hemorrhages developed. These results convince that the fibrinoid necrosis of small arteries and arterioles in the brain is the primary vascular lesion responsible for cerebral hemorrhages. 5. The incidence of the fibrinoid necrosis in small vessels was not related with the grade of high blood pressure especially during the early stage of hypertension. It was not clear, however, how much the high blood pressure itself contributed to the development of the acute arterial lesion during the advanced stage of hypertension. 6. Renal factors played a great role in producing the acute arterial lesion (fibrinoid necrosis). A renal factor other than renin seemed to be responsible for the acute arterial lesion and cerebral hemorrhages. The acute arterial lesion was induced in animals with one ischemic and the other intact kidneys during the early stage of hypertension. But, it was scarcely produced during the advanced stage of hypertension. Bilateral renal injuries (two ischemic kidneys or one ischemic kidney after one nephrectomy) enhanced the development of the acute arterial lesion. 7. High salt intake augumented the incidence of the acute arterial lesion.
社団法人日本循環器学会の論文
1973-12-20

Pathogenesis of Cerebral Hemorrhages in Experimental Hypertension in Rabbits with Particular Reference to Acute Vascular Lesions (Fibrinoid Necrosis) of Small Arteries and Arterioles

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