Abstract

Infusions of metaraminol and angiotensin were used to test the effect of increased perfusion pressure on tissue metabolism and oedema after induction of regional cerebral ischaemia in the rat and the gerbil. An increase of mean arterial blood pressure of 30-40 mm Hg in the rat over the first 2 hours after diathermy of the middle cerebral artery prevented the 100% rise in hemisphere lactate seen in normotensive control animals. Angiotensin infusion also prevented early hemispheric oedema in this model. In the gerbil, 4 hours after placing a clip on one carotid artery, metaraminol-induced increases in blood pressure had no such protective effect on the metabolic changes or on oedema. When the clip was removed after 3 hours to permit 1 hour of reperfusion, lactate levels returned to normal but the degree of oedema was unchanged. Hypertension in this reperfusion model caused a slight but not statistically significant increase in oedema. The evidence suggests that moderate increases in blood pressure may be protective against the early metabolic sequelae of focal cerebral ischaemia, but there are potential problems with oedema formation. It is argued that a clinical trial should study the potentially beneficial effects of a brief early increase in blood pressure in the acute aftermath of ischaemic stroke.