Nitric oxide does not contribute to the hypotension of heatstroke

The purpose of this study was to determine whether nitric oxide (NO) contri butes to the hypotensive state induced by prolonged environmental heat (EW) stress. Ketamine-anesthetized rats were instrumented for the measurement o f arterial blood pressure, electrocardiogram, and temperature at four sites . Rats were exposed to EH (ambient temperature, 40 +/- 1 degreesC) until me an arterial blood pressure (MAP) decreased to 75 mmHg, which was arbitraril y defined as the induction of heatstroke. In addition to cardiovascular and temperature measurements, the time required to reach this MAP end point an d the subsequent survival time were measured. In three separate experimenta l series, the competitive NO synthesis inhibitor N-omega-nitro-L-arginine m ethyl ester (L-NAME) was administered (0, 10, or 100 mg/kg) either before, during (30 min after initiation of EH), or immediately after EH. L-NAME adm inistered at any of these times transiently increased MAP. L-NAME infusion either before or during EH did not alter the EH time required to decrease M AP to 75 mmHg, but L-NAME pretreatment did decrease the colonic temperature at which this MAP end point was reached. L-NAME infusion before or after E H did not affect subsequent survival time, but L-NAME administered during E H significantly decreased survival time. The administration of L-NAME at an y time point, therefore, did not prove beneficial in either preventing or r eversing heatstroke. Taken together, these data suggest that NO does not me diate the hypotension associated with heatstroke.