Actions of nitric oxide on the acute gastrointestinal damage induced by PAF in the rat.

The actions of nitric oxide (NO) on the acute gastrointestinal damage induced by platelet-activating factor (PAF) have been investigated in the rat. S-nitroso-N-acetyl penicillamine, which spontaneously generates NO, dose-dependently inhibited PAF-induced gastrointestinal plasma leakage, a measure of the initiation of vascular damage. The inhibitor of NO synthase, NG-monomethyl-L-arginine substantially potentiated gastrointestinal damage and plasma leakage induced by E. coli endotoxin, but had no effect on that induced by intravenous infusion of PAF. Endogenous NO may thus have a protective role in the gastrointestinal vascular that can be mimicked by generators of NO. The protection afforded by endogenous NO may, however, be dependent on the nature of the inflammatory stimulus used to induce gastrointestinal damage.