The aim of this study was to investigate the effect of nitric oxide (NO) on
the gastric injury induced by hemorrhagic shock. Hemorrhagic shock was cre
ated by withdrawing 3 ml blood/200 g body weight of the rats. Before the he
morrhage, N-G-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg i.v. bolus),
D-NAME (10 mg/kg i.v. bolus), or L-arginine (100 mg/kg i.v. bolus and 10 mg
/kg/min infusion) + L-NAME were administered. At the end of the 1-hour hypo
volemic shock period, histological analysis, gastric ulcer index, gastric m
yeloperoxidase (MPO) activity, and gastric protein oxidation (PO) levels we
re determined. In histological analysis a destructive effect of L-NAME (NO
synthase inhibitor) was demonstrated. L-NAME treatment increased gastric MP
O activity, L-arginine reversed this effect and D-NAME had no effect. Tissu
e PO activity was found to be increased in L-NAME-treated rats; L-arginine
treatment reversed this activity. It is concluded that gastric barrier func
tion is altered after hemorrhagic shock, and L-arginine (NO precursor) can
prevent mucosal injury in the stomach. This effect of NO may be on gastric
blood flow and can be mediated by tissue neutrophils. Copyright (C) 2000 S.
Karger AG, Basel.