BLOOD-BRAIN BARRIER DYSFUNCTION IN ACUTE ARTERIAL HYPERTENSION AFTER PAPAVERINE-INDUCED VASODILATATION

Abstract

Vasodilatation induced by papaverine increased the vulnerability of cerebral vessels to acute hypertension as demonstrated by more extensive extravasation of Evans blue albumin and macroscopic or microscopical haemorrhages. As the tension in the vessel wall is the product of pressure and internal radius, divided by the thickness of the vessel wall, dilated precapillary resistance vessels would be exposed to higher tension than non‐dilated. Also the strain on capillaries and venules would increase because a higher pressure will be propagated to these small vessels. The results support our earlier proposal that the increased cerebrovascular permeability seen in severe acute hypertension is due to a vessel wall damage caused by rapid distension. Regional cerebral blood flow studied with ¹²⁵I‐antipyrine indicates that the flow is higher in areas with blood‐brain barrier dysfunction, further contradicting the ischaemic theory on permeability changes in hypertension.