ROLE OF ENDOGENOUS NITRIC-OXIDE IN ISCHEMIA-REPERFUSION INJURY OF RATGASTRIC-MUCOSA

It has been suggested that endogenous nitric oxide may act as a protec tive factor for gastric mucosa since nitric oxide increases blood flow and may scavenge certain oxyradicals. We tested the hypothesis that n itric oxide protects rat gastric mucosa against ischaemia-reperfusion stress. Gastric ischaemia was induced by clamping the left gastric art ery for 20 min. Rats were treated with two kinds of specific inhibitor s of nitric oxide production, N-G-nitro-L-arginine or N-G-monomethyl-L -arginine. Gastric mucosal integrity was continuously monitored by mea suring the blood-to-lumen clearance of [(51)chromium]-labelled ethylen ediaminetetraacetic acid (EDTA) under control conditions, during ischa emia and after reperfusion. Oxidative stress in gastric mucosa was ass essed by measuring dichlorofluorescein (DCF) fluorescence intensity be fore ischaemia and after reperfusion. Blockade of nitric oxide resulte d in a significant increase in [Cr-51]-EDTA clearance and DCF fluoresc ence intensity after reperfusion. These effects of nitric oxide inhibi tors were attenuated by pretreatment with L-arginine. In conclusion, t hese findings support the hypothesis that endogenous nitric oxide acts as an important protective factor against ischaemia-reperfusion stres s in rat gastric mucosa.