Cushing's mechanism maintains cerebral perfusion pressure in experimental subarachnoid haemorrhage

Mortality following subarachnoid haemorrhage (SAH) is high, especially within the first 48 h. Poor outcome is predicted by high intracranial pressure which causes diminished cerebral perfusion pressure unless a compensatory increase in mean arterial blood pressure occurs. Therefore blood pressure elevation can be protective following subarachnoid haemorrhage despite the potential for rebleeding. This study investigated blood pressure responses to SAH and the impact on cerebral perfusion pressure and outcome, as demonstrated by two experimental models. Various blood pressure responses were demonstrated, both at the ictus and within the following 5 h. Elevated MABP at the ictus and at 2 h following experimental SAH was associated with maintenance of CPP in the presence of raised ICP. Poor outcome (arrest of the cerebral circulation) was predicted by failure of MABP to increase significantly above sham levels within 2 h of SAH. Rat SAH provides relatively inexpensive models to investigate physiological mechanisms that maintain cerebral perfusion in the presence of intracranial hypertension.

► The impact of ABP responses to subarachnoid haemorrhage was assessed in two models. ► ABP usually increased at the ictus but less than the transient, maximal ICP increase. ► Failure of ABP to increase at the ictus was associated with risk of poor outcome. ► Increased ABP at 2 h was associated with maintained cerebral perfusion pressure. ► Failure of ABP to increase at 2 h was associated with poor outcome.