A brief episode of severe arterial hypertension induces delayed deterioration of brain function and worsens blood flow after transient multifocal cerebral ischemia.

Abstract

Transient arterial hypertension occurs sporadically following cerebral air embolism and may occur during the acute phase of stroke. This study used an animal model of multifocal cerebral ischemia induced by air embolism and reversed by recompression to assess the effect of induced hypertension on the evoked response recovery, local cerebral blood flow, intracranial pressure, and brain water in 19 anesthetized dogs (Canis familiaris). Six received 0.4 ml of air via the internal carotid artery, 8 received intracarotid air and 10 micrograms/kg norepinephrine to produce transient hypertension, and 5 received intracarotid saline and norepinephrine. The average evoked response recovery in the air-only group was 58.3 +/- 7.7% (mean +/- SEM) of control after 4 hours of recompression; the air plus hypertension group recovery was 15.4 +/- 2.7% (p less than 0.01). The final evoked response in the dogs receiving hypertension alone did not differ from control values. Seven of 8 dogs in the air plus hypertension group had very low blood flows; only 1 of 4 in the air-only group had very low flows. The amount of brain water and the intracranial pressure were not detectably different at the end of treatment among all 3 groups. These results support a role for endothelial damage produced by air and hypertension in potentiating the process of postischemic hypoperfusion.