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Involvement of nitric oxide (NO) in the mechanism of gastric preconditioning induced by short ischemia

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Gastric mucosa subjected to repeated brief episodes of ischemia exhibits an increased resistance to damage caused by a subsequent prolonged ischemic insult and this is called gastric preconditioning. In this study, L-NNA, a non-selective NO-synthase inhibitor, and aminoguanidine, a relative inhibitor of inducible NO-synthase (iNOS), were applied prior to short ischemia (occlusion of celiac artery 1-5 times for 5 min) followed by a subsequent exposure to 0.5 h of ischemia and 3 h of reperfusion (I/R). Short ischemia significantly reduced the I/R-induced lesions while raising significantly the GBF and luminal NO content. These effects were attenuated by L-NNA and aminoguanidine and restored by addition of L-arginine and SNAP to L-NNA and aminoguanidine. The cNOS mRNA, but not iNOSmRNA, was detected in intact mucosa and only cNOS mRNA was strongly upregulated in the preconditioned mucosa. We conclude that overexpression of cNOS with the subsequent release of NO plays a key role in the mechanism of gastric preconditioning.


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