Cerebral vasodilation capacity: acute intracranial hypertension and supra- and infra-tentorial artery velocity recording.

This experiment is the first to compare cerebral vasomotor reactivity in the supra- and infra-tentorial regions in baseline conditions and during progressive acute intracranial hypertension. The increase in intracranial pressure was performed using liquid pressure transmission in two groups of 16 rabbits by elevating a saline infusion bottle connected to the subdural space. Cerebral microvessel dilation capacity was studied using acetazolamide arterial infusion during three stages of 20 min: at baseline conditions, with an intracranial pressure value equal to half the diastolic arterial pressure and with an intracranial pressure equal to the diastolic arterial pressure. The effects of acetazolamide in the basilar artery and in the carotid siphon were simultaneously monitored by transcranial Doppler sonography during all the experiments. The changes in cerebral vasomotor reactivity occurred with the same intensity and latency in both vascular compartments in baseline conditions. The maximum amplitude of changes happened 30 s later in the basilar artery than in the carotid siphon. When intracranial pressure was above half the diastolic arterial pressure, the vasomotor tone began to decrease in the carotid siphon which supplies a small region of the rabbit brain, whereas it was maintained in the basilar artery. This effect could be explained by brain tissue hypertension. Vasomotor reactivity had nearly disappeared in all the cerebral arteries investigated when intracranial hypertension was equal to the diastolic arterial pressure. These results show evidence of a direct and late effect of acute elevation of intracranial pressure on cerebral microvascular tone. This begins in the supra-tentorial region but there is an early local effect on the carotid siphon due to the brain tissue pressure.