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  • Cited by 6
  • Print publication year: 1998
  • Online publication date: December 2009

46 - Hypertension

from Part V - Pathophysiology in disease states

Summary

Introduction

This chapter deals with blood-brain barrier dysfunction in acute and chronic hypertension and its role in the development of edematous brain lesions such as white matter changes, glial hypertrophy and morphological brain damage. The clinical relevance of experimental data is also discussed.

Acute hypertension

Blood–brain barrier (BBB) dysfunction can be observed after an acute increase in blood pressure induced by various vasoactive drugs (Johansson et al., 1970, Johansson, 1989) or by compression of the aorta (Johansson and Linder, 1974, Sokrab et al., 1988). There is no fixed level at which this occurs. Factors such as vascular tone, abruptness of the pressure increase and the drugs used all play a role. An increase in systolic pressure exceeding 60 mmHg will result in multifocal opening of the BBB to albumin in most experimental models. A number of studies have shown that the BBB dysfunction is related to vascular distension (Johansson, 1989, Table 46.1) rather than to extensive vasoconstriction – vasospasm – as earlier suggested (Byrom, 1954).

The tension in the vessel wall increases with the pressure and with the diameter of the vessels. Thus, vessels dilated by drugs or hypercapnia will be exposed to a higher stress than constricted vessels and will accordingly be more vulnerable to an increase in blood pressure (Fig. 46.1; Johansson, 1974b; 1989).