Post-ischemic neurologic recovery and cerebral blood flow using a compression model of complete "bloodless" cerebral ischemia in dogs.

Abstract

Complete "bloodless" cerebral ischemia was produced in 14 dogs by increasing intracranial pressure above systolic blood pressure (compression ischemia) for 10 min after the onset of an isoelectric EEG. Six dogs were observed for 48 h post-ischemia to assess neurologic recovery, and in 6 other dogs, acute post-ischemic cerebral blood flow was determined for 2 h. In 2 additional dogs, pre-ischemic and intra-ischemic cerebral blood volume (CBV) was measured using 111In-labeled red blood cells. Compression ischemia resulted in 2 of 6 dogs that were normal at 48 h post-ischemia, 3 dogs had moderate cerebral injury, and 1 dog died. These results were similar to results from previous studies in our laboratory in which complete "stagnant" cerebral ischemia of a comparable duration was produced in dogs using aortic and caval cross-clamping. Restoration of cerebral perfusion pressure following compression ischemia was accompanied by an initial phase of cerebral hyperemia followed by a delayed period of hypoperfusion similar to that observed following stagnant ischemia. The CBV studies in 2 dogs revealed that compression ischemia decreased CBV to 12% and 14% of pre-ischemic control values, respectively. The authors conclude, contrary to previous reports, that compression ischemia, although producing near bloodless ischemia, does not improve the brain's tolerance to ischemia.