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探讨内源性一氧化氮（NO）在大鼠应激性胃粘膜损伤中的作用及其与流基物质和脂质过氧化之间的关系。方法：建立冷束缚大鼠应激性胃粘膜损伤模型，观察：①内源性NO对胃粘膜损伤的影响；②应激后大鼠胃粘膜内巯基物质和脂质过氧化终产物丙二醛（MDA）含量的改变；③阻断NO对应激大鼠胃粘膜内上述两种物质含量的影响。结果：①外周给予NO阻断剂L－硝基精氨酸（L－NNA，12．5mg／kg）明显加重胃粘膜损伤；②应激导致胃粘膜内巯基物质含量显著降低，MDA含量明显增高；③但以L－NNA抑制内源性NO的生成，对应激大鼠胃粘膜上述两类物质的含量无明显影响。结论：内源性NO具有保护大鼠应激性胃粘膜损伤的作用，其保护作用似不通过内源性巯基物质的介导，也与胃粘膜脂质过氧化无关。
To investigate the role of endogenous nitric oxide (NO) in the stress-induced gastric mucosal injury in rats and its relationship with fluid-based substances and lipid peroxidation. Methods: The model of stress-induced gastric mucosal injury in cold-restrained rats was established. The effects of endogenous nitric oxide on gastric mucosal injury were observed. The contents of sulfhydryl and lipid peroxidation end products malondialdehyde (MDA) content changes; ③ block NO on stress gastric mucosal contents of the above two substances. Results: ① L-NNA (L-NNA, 12.5 mg / kg), a NO blocker, significantly increased gastric mucosal injury; ② The content of sulfhydryl in gastric mucosa significantly decreased and the content of MDA significantly increased ; ③ However, inhibition of endogenous nitric oxide production by L-NNA had no significant effect on the contents of these two substances in the gastric mucosa of stress rats. CONCLUSION: Endogenous nitric oxide can protect gastric mucosal injury induced by stress in rats. The protective effect of endogenous nitric oxide does not seem to be mediated by endogenous sulfhydryl groups, nor is it associated with lipid peroxidation of gastric mucosa.