EFFECTS OF NITRIC-OXIDE SYNTHASE INHIBITION ON CUTANEOUS VASODILATIONDURING BODY HEATING IN HUMANS

We sought to examine further the potential role of nitric oxide (NO) i n the neurally mediated cutaneous vasodilation in nonacral skin during body heating in humans. Six subjects were heated with a water-perfuse d suit while cutaneous blood flow was measured by using laser-Doppler flowmeters placed on both forearms. The NO synthase inhibitor N-G-mono methyI-L-arginine (L-NMMA) was given selectively to one forearm via a brachial artery catheter after marked cutaneous vasodilation had been established. During body heating, oral temperature increased by 1.1 +/ - 0.1 degrees C while heart rate increased by 30 +/- 6 beats/min, Mean arterial pressure stayed constant at 84 +/- 2 mmHg. In the experiment al forearm, cutaneous vascular conductance (CVC; laser-Doppler) decrea sed to 86 +/- 5% of the peak response to heating (P < 0.05 vs. pre-L-N MMA values) after L-NMMA infusion. In some subjects, L-NMMA caused CVC to fall by similar to 30%; in others, it had little impact on the cut aneous circulation. CVC in the control arm showed a similar increase w ith heating, then stayed constant while L-NMMA was given to the contra lateral side. These results demonstrate that NO contributes modestly, but not consistently, to cutaneous vasodilation during body heating in humans. They also indicate that NO is not the only factor responsible for the dilation.