The consequences of cerebral venous circulatory disturbances associated with brain ischemia.

The aim of this study was to test the effects of interference with venous return from the brain on the brain damage produced by occlusion of the middle cerebral artery (MCA-O). Tests were performed in anesthetized, artificially ventilated rats. The extent of the infarction produced in the hemisphere ipsilateral to the occluded middle cerebral artery (MCA) was less in rats in which cerebral venous return had been disrupted by bilateral ligation of the external and internal jugular veins. The blood flow of a sample cortical area ipsilateral to the MCA-O (measure by a laser Doppler flowmeter) decreased less, during a 45 min MCA-O, in the group with venous return interference. The blood concentration of the marker of CNS damage (the S-100 protein), measured 24 hrs after the end of the 45 min MCA-O, was lower in the rats with venous return interference. In order to be effective, the interference with venous return had to start before, and be concurrent with, MCA-O. When the interference with venous return started during the period of MCA-O, the brain damage was enhanced and resulted in death of the animals within 24 hrs post-occlusion. It is concluded that increasing brain venous pressure may, under some conditions, protect brain tissue against ischemic damage.