A primate model of subarachnoid hemorrhage: change in regional cerebral blood flow, autoregulation carbon dioxide reactivity, and central conduction time.

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Abstract
An experimental model of subarachnoid hemorrhage was developed in the baboon to allow accurate measurements of the changes of ICP [intracranial pressure] and cortial blood flow, autoregulation, reactivity changes and central conduction time extending over a period up to 3 mo. Hydrogen electrodes (12) were implanted in pairs allowing CBF [cerebral blood flow] measurements in standard areas A, B, C of each hemisphere. Bleeding was produced by the transection of the posterior communicating artery with a specially constructed snare. The snare was implanted by the transorbital route, and measurements were made in 6 animals and subarachnoid hemorrhage produced in 5. All animals survived and were graded clinically after 48 h as grade I, 1 animal; grade II, 2 animals; grade III, 1 animal; and grade IV, 1 animal. Transection of the artery produced a dramatic rise in ICP in all 5 animals, reaching a mean value of 90 mm Hg. The cerebral perfusion pressure was preserved in all 5 animals but reduced to an average of 37% normal. The CBF fell dramatically within 10 min following bleed in all animals. Thereafter, 2 patterns of change were established. In grade I and II animals there was an immediate rapid recovery in CBF significantly exceeding prebleed values. A 2nd hyperemic peak was observed 2 days after the bleed. In grade III and IV animals the initial postbleed recovery was limited and a 2nd hyperemic peak did not occur. The most significant reduction in CBF was recorded in both grade III/IV animals in regions A (operculum), corresponding to their hemiparesis. There was also a depresion in CBF in other areas in the grade IV animal. CCT [central conduction time] was significantly prolonged in both grade III and IV animals. The prolongation was most prominent 2 days after the bleed. Autoregulation was globally depressed in all 5 animals without regional differences. At 48 h, animals in grade I and II showed better recovery than those in grade III and IV. Reactivity to pCO2 [partial pressure of CO2] was regionally depressed in areas corresponding to neurological deficit only in grade III and IV animals. These observations are believed to relate to clinical practice in the management of patients after subarachnoid hemorrhage. Apparently, posthemorrhagic hyperemia is a favorable prognostic sign. Prolongation of CCT may indicate an ischemic incident in a clinicially affected animal, and disturbance of autoregulation and reactivity justify the use of arterial hypertension and controlled ventilation in some cases following aneurysmal surgery.