Influence of L-NAME and L-Arg on ischaemia-reperfusion induced gastric mucosa damage

Objective : The aim of this study was to investigate effects of L-NAME and L-Arginine on gastric mucosal injury induced by ischaemia-reperfusion. Methods : In the experiment, 20 New Zealand rabbits were used (2700-3000 g). Celiac artery was clamped for 30 min for ischaemia and then 60 min of reperfusion followed this after all rabbits were anaesthetized. In the Sham-control group (G 1, n = 5), laparotomy was performed, and the celiac artery was prepared without clip- ping. Group 2 (Untreated, n = 5) rabbits were only subjected to ischaemia-reperfusion. Group 3 (n = 5) rabbits had L-Arginine Methyl Ester (L-Arg) 3 mg/kg/min as IV infusion during the first 15 min of the reperfusion. Group 4 (n = 5) rabbits had a nitric oxide inhibitor NG-nitro-L-arginine methyl ester (L-NAME) 100 µg/kg/min IV during the first 15 min of the reperfusion. After 60 min of reperfusion, the rabbits were killed, and their stomachs were removed for histopathologic evaluation and determination of malondialdehyde (MDA) level. Results: After ischaemia-reperfusion, Untreated group had macroscopic necrosis involving 50 ± 6% of total gastric mucosa area and deep mucosal necrosis involving 10 ± 5% of mucosal strips. In the group treated with L-NAME, macroscopic mucosal necrosis involved 52 ± 6% of total gastric mucosa area and deep mucosal necrosis involved 11 ± 3% of mucosal strips (both p > 0.05 versus Untreated group). L-Arg treatment significantly reduced macroscopic mucosal necrosis area to 20 ± 6% and deep mucosal necrosis to 3 ± 1% (both p < 0.05 versus Untreated group and L- NAME group). MDA level in the L-Arg group was significantly lower when compared to control and L-NAME group MDA level (p < 0.05). Conclusion : These results suggest that NO increase induced by L-Arginine injection is involved in the protection of gastric mucosa after ischaemia-reperfusion. (Acta gastroenterol. belg., 2002, 65, 150-154).