Cerebral infarction due to carotid occlusion and carbon monoxide exposure. I. Pathophysiological and neuropathological investigations.

Abstract

Series IAfter anaesthesia with diethyl-ether one common carotid artery was ligated and transsected. Twenty-four hours later the animals were exposed to carbon monoxide (3000 ppm in room air) for 90 minutes while held in a plastic box with a volume of 3001, allowing the exposure of eight animals at a time. The gas mixture was stirred by a fan. The concentration of carbon monoxide was continuously monitored inside the plastic container and in its immediate vicinity by an infrared spectrometer (URAS I, Hartmann & Braun, FRG) to assure a continuous exposure of the animals and to protect laboratory personnel against accidental leaks. At the 48th hour after exposure the rats were anaesthetised with diethyl-ether and perfused via the ascending aorta with formalin after briefly washing out the vasculature with saline.

Erythropoietin in the treatment of carbon monoxide neurotoxicity in rat

“…Calculations were based on the external standard (62.5e500 ng/ml) in the same solvent. The data were expressed in terms of Evans blue mg/wet tissue weight (g) (Laas et al, 1983).…”

“…Extravasations of Evans blue due to blood brain barrier damage were determined using a fluorometric method (Laas et al, 1983). Briefly, the brain was quickly removed, homogenized in 1.5 ml of 50% trichloroacetic acid (w/v), and then centrifuged at 1500Â g for 20 min.…”

Ischemic Brain Damage Induced by Repeated Brief Occlusions of Bilateral Common Carotid Artery in Rats.

“…Various complex methods have been advanced to induce experimental ischemia in the rat brain which is rich in collateral circulations (Pulsinelli and Brierley 1979;Laas et al 1983;Mendelow et al 1984; Kameyama et al 1985; Chen et al 1986). Although occlusion of the unilateral carotid artery little disturbs the cerebral blood flow and metabolism in the rat (Garcia 1984), permanent ligation of the bilateral common carotid artery has been shown to induce severe ischemic damage in the rat brain (Payan et al 1965;Ogata et al 1976).…”