Acute model of gastric mucosal damage induced by perfusion of the 70% ethanol in to stomachwas estab1ished. Gastric mucosal blood flow(GMBF), transmucosal potential difference(PD) and gastric mucosal lesion indices and the contents of nitric oxide (NO) in blood and gastric mucosal were detected. The protective effect of moxibustion(M) on gastric mucosal damage in rats and the relationwith nitric oxide were studied. The results obtained were as follows: 1) M has protective effect on gastric mucosal damage in rats. 2) Both precursor of NO-L-arginine(L-arg) and donor of NO-natrii nitroprussidum(SNP) also has the protective effect on gastric mucosal damage in rats. But NO synthesis inhibltor-NG-nitric-L-arginine(L-NNA) could not have the gastroprotective effect. 3 ) By both pretreatment of L-arg and SNP, the gastroprotective effect of M was increased, but by pretreatment of L-NNAand L-arg, the gastroprotective effect was reversed. However, by pretreatment of I,-NNA, the gastroprotective effect of M was decreased. Conclusion: the protective effect of M on gastric mucosal damagein rats was mediated through activation of L-arg-NO
In this paper, we analysed the changes of NO contents in serum and gastric mucosa in experimental ulcer rats treated by moxibustion, and observed its effect on L-NNA inhibition. The results showed:NO contents in gastric ulcer rats were increased, especially the contents of NO in gastric mucosa werehigher than that of the normal control group, P< 0. 05. After moxibustion the NO level was decreased,tending to the normal level, among them the changes of NO in serum had statistical significance, P< 0.05. By injection of L-NNA the NO contents in gastric ulcer rats showed a tendency to decrease. Aftermoxibustion no was more decressed. It suggested that NO participating in the treatment of moxibustiongastric ulcer might be due to a protection against the damage of gastric mucosa caused by the propertiesof vascular relaxation. Moreover, moxibustion could strengthen L-NNA inhibition on the synthesis
