Acute experimental hypertension induced by clamping of the thoracic aorta resulted in blood-brain barrier dysfunction as revealed by extravasation of Evans blue-albumin in 10 out of 13 dogs. The tracer distribution was similar to that found in animals with metaraminol-induced hypertension, which supports the hypothesis that the high intravascular pressure per se and not any toxic drug effect is the factor that brings about increased permeability to protein tracers.
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Johansson et al. (2009) studied this question.
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