Evidence that disruption of the blood-brain barrier precedes reduction in cerebral blood flow in hypertensive encephalopathy

Abstract

Alternative hypotheses concerning the pathogenesis of hypertensive encephalopathyare that vasospasm produces cerebral ischemia and cerebral edema, or that passive dilation ofcerebral vessels during severe hypertension produces disruption of the blood-brain barrier andcerebral edema. Stroke-prone spontaneously hypertensive rats (SHRSP) were studied when theydeveloped signs of neurological dysfunction. We measured regional cerebral blood flow (rCBF) withl4C-iodoantipyrine, and permeability of the blood-brain barrier with Evans blue dye. Twelve rats hadfocal disruption of the barrier without histological evidence of ischemic infarction or cerebral hemorrhage:areas with disruption of the barrier had severe focal edema in seven rats and minimal edema infive rats. In areas with disruption of the barrier and marked focal edema, rCBF was decreased to 38± 8 (mean ± SE) ml/min/100g vs 102 ± 13 (p< 0.05) in other areas of the ipsilateral hemisphere, and86 ± 16 in the homologous area of the contralateral hemisphere (p < 0.05). In contrast, in areas withdisruption of the blood-brain barrier with only minimal edema, rCBF was normal or increased: rCBFwas 100 ± 11 ml/min/100 g vs 85 ± 12 in other areas of the ipsilateral hemisphere (p > 0.05) and 64 ±8 in the homologous area contralaterally (p < 0.05). The findings indicate that edema precedesreduction in rCBF in SHRSP and suggest that the initiating event in hypertensive encephalopathy isdisruption of the blood-brain barrier, and not vasospasm © 1984 American Heart Association, Inc.