The pathogenesis of ischaemic neuronal damage along the cerebral arterial boundary zones in Papio anubis.
The pathogenesis of ischaemic neuronal damage along the arterial boundary zones of the forebrain was investigated in 20 lightly anaesthetized, spontaneously breathing baboons. A combination of bilateral common carotid artery occlusion and systemic hypoxia was used. An arterial PO2  of 21.2 +/- 2.5 mmHg was maintained for about 20 min. Additional occlusion of the left common carotid artery for 20 min had no effect on the EEG (except for one animal with a cerebrovascular anomaly). Only when occlusion of the right carotid artery was added did the EEG become almost or completely isoelectric after an interval ranging from 23 s to 44 min (sequential common carotid artery occlusion while breathing air did not affect the EEG). After a chosen period of electrical silence, hypoxia and carotid occlusion were terminated. Hypotension did not occur during carotid occlusion or the recovery period. Survival was deliberately limited to 46 h, during which neurological assessment was made and the EEG was recorded just before in vivo perfusion-fixation of the brain. Neurological deficits included asymmetrical quadriparesis and myoclonus epilepsy. The brains of 3 animals were normal and in the 15 with brain damage this was restricted in the cerebral cortex to the arterial boundary zones. In the presence of profound hypoxia the oligaemia due to bilateral carotid occlusion can reduce tissue oxygenation locally to a level critical for the production of ischaemic damage in the cortical boundary zones. Portions of the basal ganglia were also involved in 7. The quantified brain damage scores correlated with the EEG scored on a six-point scale during the perod of electrical silence and early recovery. Brain damage scores also correlated with the times for intracranial pressure to return to normal levels from the peaks recorded just after the end of arterial occlusion and hypoxia. As brain damage only occurred when the EEG during bilateral carotid occlusion and hypoxia was silent for at least 8 min, it was concluded that in a variety of clinical settings a simple EEG-based monitoring system would be optimal for the detection of an impending failure of cerebral oxygen supply.
D000818:Animals; D001794:Blood Pressure; D001921:Brain / Q000473:pathology; D001925:Brain Damage, Chronic / Q000473:pathology / Q000503:physiopathology*; D002545:Brain Ischemia / Q000473:pathology / Q000503:physiopathology*; D002245:Carbon Dioxide / Q000097:blood; D002339:Carotid Arteries / Q000503:physiopathology; D002536:Cerebral Arteries / Q000503:physiopathology; D002540:Cerebral Cortex / Q000503:physiopathology; D005260:Female; D002534:Hypoxia, Brain / Q000503:physiopathology; D008297:Male; D009474:Neurons / Q000502:physiology; D010100:Oxygen / Q000097:blood; D010215:Papio
D002245:Carbon Dioxide; D010100:Oxygen