A primate model of subarachnoid hemorrhage: change in regional cerebral blood flow, autoregulation carbon dioxide reactivity, and central conduction time.
SUMMARY 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 IV — one 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 pC02 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. Stroke, Vol 13, No 5, 1982 ANEURYSM SURGERY forms a large and technical becomes relevant to the maintenance of cerebral perfu ly demanding part of neurosurgical practice, and de sion pression (CPP). spite the technical advances, 1 the fate of the patient is The best combination of therapy in an individual still dependent on the stability and reserves of the cere patient is often elusive, because the reactivity and au bral circulation before and after surgery. The uncer toregulatory capacity of the damaged cerebral circula tainty of treatment of circulatory disturbance following tion is unknown. The present experiments were de subarachnoid haemorrhage (SAH) is manifest by the signed to produce a primate model of SAR that plethora of therapeutic advice in the literature. reproduces the changes following human aneurysmal The management of arterial narrowing, ischaemia SAH as closely as is possible in a laboratory model. and oedema depend on a knowledge of the disordered The parameters to be measured following the haem physiology of the cerebral circulation produced by an orrhage are those difficult to measure accurately in eurysm rupture. The major therapeutic possibilities to humans. Central conduction time, changes in ICP dur minimise ischaemia that may follow subarachnoid ing initial bleed, regional blood flows in cortical tissue haemorrhage (SAH), are limited to manipulation of and the assessment of reactivity and autoregulation in systemic blood pressure, alteration of blood volume damaged areas are of particular interest. Measure and viscosity, and control of arterial carbon dioxide ments need to be continued for days and weeks after tension. If ischaemic oedema supervenes, control of the SAH to allow conclusion to be relevant to patients intracranial pressure (ICP) and blood pressure (BP) commonly presenting many hours after the ictus, and operated upon some day later.
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