The effect of the BBB opening to proteins on development of post-ischemic brain injury was assessed in 32 cats subjected to one hour MCA occlusion. The CBF was measured by hydrogen clearance from electrodes inserted in the caudate and the cerebral cortex within the MCA territory. In 16 animals, a prevention of subsequent ractive hyperemia was attempted by hypovolemia, produced by withdrawal of blood just before the release of MCA occlusion. The hypovolemia was successful in prevention of post-ischemic hyperemia in five out of eight cats sacrificed at 3 hr and in six out of eight animals killed after 3 and 14 days. In cats sacrificed 3 hr after release of MCA occlusion, ischemic sites, associated with reactive hyperemia, showed evidence of BBB breakdown to proteins and significantly more severe edema than at the ischemic sites without reactive hyperemia, which otherwise failed to reveal leakage of EB tracer. In the cats sacrificed at 3 and 14 days, the ischemic sites which showed reactive hyperemia after release of MCA occlusion, revealed much more severe ischemic brain tissue injury than was observed at the sites without reactive hyperemia, which also did not show any EB leakage. In animals, which during the MCA occlusion showed similar intensity of ischemia in the caudate and the cerebral cortex, revealed usually more pronounced hyperemia in the former. The post-ischemic edema and the ischemic tissue injury appeared to be generally more severe in the caudate than in the cerebral cortex. The present studies indicate that reactive hyperemia, which follows release of major cerebral artery occlusion, may play a significant role in the breakdown of the BBB to proteins, and in increasing the severity of post-ischemic edema and of ischemic brain tissue injury.
