Altered membrane properties of cerebral vascular smooth muscle following subarachnoid hemorrhage: an electrophysiological study. I. Changes in resting membrane potential (Em) and effect on the electrogenic pump potential contribution to Em.

Subarachnoid hemorrhage was produced experimentally in cats by intracisternal injection of non-heparinized autologous arterial blood obtained by cardiac puncture under ketamine and xylazine anesthesia. Cats were sacrificed at varying time intervals between 30 min and 7 days post ictus. Measurements of resting membrane potential were recorded from smooth muscle cells of the basilar artery. These measurements were obtained by impalement from the adventitial surface of isolated but otherwise intact segments of the artery using glass microelectrodes with tip sizes less than 0.1 micron. The resting membrane potential recorded in vitro from animals previously subjected to subarachnoid hemorrhage in vivo was consistently and significantly depolarized when compared to normal controls. This depolarization was present as early as 30 min post ictus. Addition of the cardiac glycoside, ouabain, in a concentration of 10(-5)M depolarized cells from both control and experimental animals. There is a significant electrogenic pump potential contribution to the resting membrane potential of vascular smooth muscle cells. Ouabain is a potent blocker of Na+, K+-ATPase, the enzyme responsible for maintaining the cation electrochemical gradients. The depolarization recorded in these cells following subarachnoid hemorrhage is not, therefore, due to impairment of the electrogenic pump. The significance and implications of these findings are discussed.