Brain capillary lesions produced by cocaine in rats.

In the last 20 years, acute and chronic cocaine addiction has increased among young and adult people. The effects of cocaine on brain vasculature of young animals have not been histologically studied in depth. In the present study, we report the lesions of brain capillaries, including the choroid plexus, produced by chronic cocaine administration, in adult Wistar rats receiving i.p., 30 mg/kg/day of aqueous cocaine hydrochloride solution. Rats were sacrificed after several days of treatment. Histopathological examination of capillaries from different brain regions and cerebellum was performed using light microscopy. At 7 days, there were initial signs of dilatation, rupture and thrombosis of capillaries. At 15 days of treatment small interstitial oedema and hemorrhages by rupture of the basal membrane of the capillaries was found. At 30 days of treatment, many capillaries from different areas showed fibroid endothelial thickening, and wall fibrosis become evident after 60 days of daily cocaine. In numerous places (cortex, gray nucleus: thalamus, caudate, hippocampus and cerebellum) we observed capillaries with an occluded lumen probably due to fibrosis or thrombi after 90 days of treatment. In the latter treatment, capillaries from the choroid plexuses had their lumen dilated and the epithelial cells vacuolated or necrotic. We hypothesize that the chronic administration of cocaine in rats induced brain lesions in part as a result of capillary disruption and subsequent extravasation of erythrocytes to brain parenchyma.