Participation of nitric oxide in the mustard oil-induced neurogenic inflammation of the rat paw skin.

The possibility of nitric oxide (NO) participating in the neurogenic inflammatory reaction of the rat hindpaw skin to topical application of mustard oil was examined in anesthetized rats. Vasodilation was measured by contactless infrared emission thermography, plasma protein exudation was measured by the Evans blue leakage technique, and formation of oedema was determined by measurement of the paw volume. Topical administration of mustard oil increased the temperature of the paw skin by 2-3 degrees C, a response that was accompanied by plasma protein extravasation and followed by development of slight oedema amounting to a 7-8% increase in paw volume. That the mustard oil-induced increase in paw temperature and oedema formation was neurogenic was shown by the finding that both responses were absent in adult rats treated with a neurotoxic dose of capsaicin (0.16 mmol kg-1 s.c.) as neonates. NG-Nitro-L-arginine methyl ester (L-NAME, 43 mumol kg-1 i.v.) an inhibitor of NO formation, caused a significant increase in mean arterial blood pressure and a moderate decrease in cutaneous blood flow, whereas the same dose of the inactive enantiomer, D-NAME, was without effect. L-NAME, but not D-NAME, reduced the cutaneous hyperaemia caused by topical administration of mustard oil by about 50% but did not significantly diminish the exudative reaction to mustard oil. These findings indicate that endothelium-derived NO plays a mediator role in the vasodilator component of mustard oil-induced neurogenic inflammation in the rat paw skin whereas the increase in vascular permeability does not seem to involve NO directly as a mediator.