The Cerebral Collateral Circulation

Abstract

Studies of cerebral cortical ischemia in the monkey by direct observation and photography of pial vessels in conjunction with electropolarographic records of cortical tissue oxygen availability in the same area showed that ischemic anoxia to the point of failure of eeg and production of injury potential could be reversible without structural damage. Owing to the effectiveness of collateral circulation blood flow continued in all vessels in the area during ischemia due to clamping a main vessel. Only with catastrophic failure of the circulation does flow cease in smaller arterioles and then first in anastomotic vessels. With prolonged occlusion of the middle cerebral artery and poor collateral circulation the first change other than alteration of diameter of vessels appears after 5 minutes in the form of stasis in small venules emerging from the cortex at isolated discrete points. This "venous micro-stasis" was reversible within 15-30 minutes by increasing blood pressure, otherwise it remained. It was more difficult to produce if the animal had been heparinized. Venous micro-stasis was associated with edema and transudate of trypan blue from vessels surrounding the focus. Further ischemia enlarged the underlying area of capillary stasis, involving neighboring emergent venules. Repeated or continued ischemia resulted in confluent stasis with infarction. This type of infarction results from all types of vascular occlusion at a distance, including embolism, instances of which were observed. The primary event was considered to be endothelial damage to capillaries, for the venous microstasis was also produced by anoxic anoxia (nitrogen breathing). Thrombosis appeared to play no part in the early stages of obstruction of cortical vessels in an area of ischemic damage.