Pial Venous Reaction to Sympathetic Stimulation During Elevated Intracranial Pressure

Summary

Earlier experiments have shown that a sympathoadrenergic mechanism is able to decrease intracranial pressure by venous constriction and a consequent reduction in cerebral blood volume. In the present study using 16 cats, the intracranial pressure was elevated by two different models (cisternal infusion of mock CSF in 8 cats and brain oedema induced by water-intoxication in 8 cats) to test the hypothesis that cervical sympathetic stimulation is also effective under the circumstance of an elevated ICP. A cranial window technique and multichannel-videoangiometry were used to measure variations in pial venous calibres. The elevation of ICP up to 30 mmHg with brain oedema and 50 mmHg with CSF-infusion per se resulted in marked venous and arterial dilatation in the first model and arterial dilatation only in the second model. Pial venous constriction induced by sympathetic stimulation was significantly less with an elevated ICP. ICP reduction as a consequence of vascular constriction during stimulation remained around 15% between the resting condition and the situation of ICP elevated to 30 mmHg by CSF infusion; at higher ICP levels up to 50 mmHg, the percent ICP reduction with sympathetic stimulation fell to 10%.

The results indicate that the sympathoadrenergic system exerts a regulatory influence on cerebral blood volume via alterations in venous calibre both at a normal and increased ICP. The clinical importance of this mechanism for the control of an elevated ICP may, however, be limited.