Cerebral infarction due to carotid occlusion and carbon monoxide exposure III. Influence of neck vein occlusion.

Abstract

SUMMARY Unilateral cerebral infarcts were produced in the rat by ligation of one common carotid artery and a subsequent exposure to carbon monoxide. In animals which had undergone an additional ligation of the external jugular veins leading to a moderate increase of the cephalic venous pressure the outcome of the procedure was ameliorated significantly. Venous pressure elevation was thought to reduce the venous vascular resistance effectively by preventing the leptomeningeal veins from collapsing. Collapse of the leptomeningeal veins probably occurred during the severe carbon monoxide-induced hypotension causing a steep increase of cerebral vascular resistance.There is evidence that the threshold value of cerebral perfusion pressure below which cerebral infarcts occur is conspicuously clear-cut.' 2 We presume that this in part can be attributed to the collapse of leptomeningeal veins, which is known to increase flow resistance. Since a collapsed vessel can be distended by adding a flow resistance to its outlet we tested the hypothesis that the incidence of hypotension-induced brain lesions could be reduced by elevating the cephalic venous flow resistance. We used a modified Levine procedure which has been described in detail.3 Material and methodsThe experiments were perfonned with unstarved male albino rats of the Chbb:THOM strain. Series IIn 88 of 175 animals (body weight: 300-400 g) both external jugular veins were ligated at the time of unilateral common carotid artery ligation. Twenty-four hours later the carbon monoxide exposure (3000 ppm in room air, 90 minutes duration) was performed.