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.