Nitric oxide increases cutaneous and respiratory heat dissipation in conscious rabbits.

The influence of systemic nitric oxide (NO) donor infusion and NO synthase inhibition on major thermoregulatory mechanisms was investigated under thermoneutral conditions (24 degrees C) in the conscious rabbit. Both low (25 nmol.min-1.kg-1) and high-dose (75 nmol.min-1.kg-1) infusion of the NO donors 3-morpholinosydnonimine-hydrochloride and S-nitroso-N-acetylpenicillamine augmented respiratory heat dissipation due to raised respiratory frequency (RF) and evaporative water loss (REWL). At the higher dose of NO donor, RF and REWL increased (from 107 +/- 16 to 156 +/- 19 breaths/min and from 7.12 +/- 0.97 to 11.29 +/- 1.29 mg.min-1.kg-1; P < 0.05), and, combined with a moderate rise in cutaneous heat dissipation (ear skin temperature increased from 29.03 +/- 1.76 to 33.29 +/- 2.71 degrees C; P < 0.05), deep body temperature was slightly reduced (-0.1 degrees C, P > 0.05) without a change in metabolic heat production. In contrast, blockade of endogenous NO synthesis induced a sustained rise in body temperature (0.2 degrees C, P < 0.05), concomitant with a reduction in both RF and REWL (from 131 +/- 11 to 94 +/- 12 breaths/min and from 10.86 +/- 1.14 to 8.70 +/- 0.88 mg.min-1.kg-1, P < 0.05), whereas metabolic heat production decreased slightly and cutaneous heat dissipation was minimally altered. The data indicate that, under thermoneutral conditions, systemically applied NO primarily influences body temperature in the conscious rabbit by modulating the rate of respiratory heat dissipation, whereas the roles of cutaneous heat dissipation and metabolic heat production are relatively minor.