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

Ligation of one common carotid artery and exposure to carbon monoxide has proved to be a reliable method of producing unilateral cerebral infarcts in the rat, allowing controlled experiments in any given sample size. Pathophysiological measurements in awake and narcotized rats has shown that, in contrast to hypoxic hypoxia, the carbon monoxide-induced functional anaemia (3000 ppm in room air) did not stimulate chemoreceptors, thus causing a severe systemic hypotension owing to peripheral vascular dilatation. This hypotension is likely to represent the main pathogenetic factor in this model. An inhibition of ferro-enzymes by carbon monoxide did not seem to be involved. The only cause of death was shown to be diffuse ipsilateral brain oedema with or without extra-vasation of serum proteins. The EEG, the systemic arterial pressure, rotational behaviour, and carotidal stump pressure proved to be reliable predictors of outcome.