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

Abstract

An experimental model of subarachnoid haemorrhage has been developed in the baboon to allow accurate measurements of the changes of ICP and cortical bloodflow, auto-regulatiion, reactivity changes and central conduction time extending over a period up to three months. Twelve hydrogen electrodes were implanted in pairs allowing CBF measurements in standard areas A, B, C of each hemi sphere. 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 six animals and subarachnoid haemorrhage produced in five. All animals survived and were graded clinically after 48 hours as Grade I -one animal; Grade II -two animals; Grade III -one animal; and Grade IVone animal. Transection of the artery produced a dramatic rise in ICP in all five animals, reaching a mean value of 90 mm Hg. The cerebral perfusion pressure was preserved in all five animals but reduced to an average of 37% normal. The CBF fell dramatically within 10 minutes following bleed in all animals. Thereafter two patterns of change were established. In Grade I and II animals there was an immediate rapid recovery in CBF significantly exceeding pre-bleed values. A second hyperaemic peak was observed two days after the bleed. In Grade III and IV animals the initial post-bleed recovery was limited and a second hyperaemic 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 depression in CBF in other areas in the Grade IV animal. CCT was significantly prolonged in both Grade III and IV animals. The prolongation was most prominent two days after the bleed. Autoregulation was globally depressed in all five animals without regional differences. However, at 48 hours, animals in Grade I and II showed better recovery than those in Grade III and IV. Reactivity to pC0 2 was regionally depressed in areas corresponding to neurological deficit only in both Grade III and IV animals. We believe that our observa tions relate to clinical practice in the management of patients after subarachnoid haemorrhage and that 1. post-haemorrhagic hyperaemia is a favourable prognostic sign, 2. prolongation of CCT may indicate an ischaemic incident in a clinically affected animal, and 3. disturbance of autoregulation and reactivity justify the use of arterial hypertension and controlled ventilation in some cases following aneurysmal surgery.