Influence of experimental chronic hypertension on the cerebral and renal arteries of wild cats.

The influence of chronic hypertension (HT) on the cerebral and renal arteries was examined pathologically and morphometrically in wild cats without a specific genetic background. Chronic HT for 8-15 months was induced by uninephrectomy and salt-loading, and the blood pressure was monitored for a maximum of 5 months. The grade of systolic blood pressure elevation in each cat during the monitoring period was 21-51 mmHg. Histologically, the cerebral arachnoid and medullary arteries of all hypertensive cats showed a well-preserved medial layer, and neither loss of medial smooth muscle cells, adventitial fibrosis or fibrinoid exudation was detected. This experimental model of chronic HT in wild cats for 8-15 months induced segmental intimal elastofibrosis of the arachnoid and renal arteries, but spared the cerebral medullary artery. The parenchymal changes in the brain were negligible. Morphometrically, the arachnoid artery in control cats had a significantly thinner media than the renal artery, and the medial hypertrophy of the arachnoid artery resulting from HT occurred significantly less frequently than that of the renal artery. These findings suggest that the arachnoid and medullary arteries are relatively well protected from HT, and that this may be characteristic of cerebral arteries in general and ascribed to autoregulation.

Neuropathological study of the role of mast cells and histamine-positive neurons in selective vulnerability of the thalamus and inferior colliculus in thiamine-deficient encephalopathy.

The purpose of the present study was to examine the role of histamine in the pathogenesis of experimental thiamine-deficient encephalopathy. By studying sagittal serial sections the authors were able to examine the topographical relationship between histamine-positive neurons and fibers, the number of mast cells, and localized lesions in the thalamus (TH) and inferior colliculus (IC). Adult rats were given a thiamine-deficient diet and pyrithiamine was given intraperitoneally (30 microg/100 g bodyweight per day), and the distribution of vulnerable regions and petechial bleeding was histologically examined by reconstruction of the sagittal serial sections. The distribution of mast cells and histamine-positive neurons and fibers was examined immunohistochemically in control rats, and compared between the vulnerable and non-vulnerable regions of the TH and tectum. Changes in the aforementioned measures during the thiamine-deficient state were also examined. The blood-brain barrier was examined using antibodies against rat endothelial barrier antigen (EBA) and albumin. The density of histamine-positive fibers in the vulnerable regions of the TH and IC was very low and not different from the non-vulnerable regions, and the number of mast cells was significantly higher in the lateral portion of the TH than the medial portion of the TH. The numbers of mast cells increased on days 7-10 after the start of the experiment, and significantly decreased on days 14-21. Histamine-positive neurons and fibers in the TH and IC also had the same changes. Bleeding of the IC occurred exclusively around arteries, and perivenous bleeding was absent. Albumin exudation and suppression of EBA expression of capillaries were found in the spongy lesions of the TH and IC. The role of histamine in selective vulnerability of the TH and IC in experimental thiamine-deficient encephalopathy was not supported. Findings in the present study suggest that the spongy change is a primary event, and vascular changes are secondary.