Abstract
Porcine cerebral arterial strips denuded of the endothelium responded to transmural electrical stimulation (5 Hz for 40 s) with a relaxation, which was abolished by tetrodotoxin and N G-nitro-L-arginine, a NO synthase inhibitor. Lowering the temperature of the bathing media from 37°C to 33°C or 25°C potentiated the response to nerve stimulation, but did not affect relaxations induced by NO applied exogenously. Hypoxia suppressed the stimulation-induced relaxation at 37°C, but hypothermia blunted the inhibitory effect of hypoxia in a temperature-dependent manner. It is concluded that hypothermia augments vasodilatation associated with nitroxidergic (nitrergic) nerve activation possibly by increasing the production of NO from L-arginine and, in addition, prevents impairment of NO production by hypoxia. These mechanisms likely explain how hypothermia protects nerve cells against hypoxia. Inhibitions of cyclic GMP phosphodiesterase and of superoxide production by hypoxia do not seem to participate in the action of hypothermia. Mechanisms underlying its protective action remain to be ascertained.
