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目的 :探讨内源性 NO对应激性胃粘膜损伤的保护作用及其机制。 方法 :以浸水束缚应激造成大鼠急性胃粘膜损伤 ,用溃疡指数 (U I)反映粘膜损伤程度 ,Griess法检测血浆及粘膜 NO含量 ,L DF- 3型激光多谱勒血流仪监测胃粘膜血流量(GMBF)的变化 ,并分别以左旋精氨酸甲酯 (L - NAME)及左旋精氨酸 (L - Arg)抑制或促进内源性 NO的合成 ,观察 UI的变化。 结果 :浸水束缚应激 4h可致严重的胃粘膜损伤 ,同时粘膜血流量明显下降 ,血浆及粘膜 NO含量明显升高 ,与正常对照组相比差异非常显著 (P<0 .0 1) ;L - NAME明显加重粘膜损伤 ,并阻抑了应激所致的血浆及粘膜内 NO含量的升高 ,使粘膜血流量更趋下降 ,与实验对照组相比差异显著 (P<0 .0 5 ) ;L - Arg可明显升高粘膜血流量及血浆、粘膜内 NO含量 ,明显减轻粘膜损伤程度 ,与实验对照组相比差异非常显著 (P<0 .0 1)。结论 :内源性 NO对应激性胃粘膜损伤具有保护作用 ,抑制或促进其合成 ,可加重或减轻粘膜损伤 ,这一作用是通过影响粘膜血流量实现的。
Objective: To investigate the protective effect of endogenous nitric oxide on gastric mucosal injury and its mechanism. Methods: Acute gastric mucosal injury was induced by water immersion restraint stress. Ulcer index (UI) was used to detect the degree of mucosal injury. Plasma and mucosal NO contents were detected by Griess method. Gastric mucosa was monitored by L DF-3 laser Doppler flowmeter (GMBF). The changes of endogenous NO were inhibited or promoted by L - NAME and L - Arginine respectively. The changes of UI were observed. Results: Immersion restraint stress for 4h caused severe gastric mucosal damage, meanwhile the mucosal blood flow decreased significantly and the content of NO in plasma and mucosa significantly increased compared with the normal control group (P <0.01); L - NAME significantly aggravated mucosal injury and inhibited the increase of NO content in plasma and mucosa induced by stress, which decreased the mucosal blood flow more significantly compared with the experimental control group (P <0.05) L - Arg significantly increased mucosal blood flow and NO content in plasma and mucosa, and significantly reduced the degree of mucosal injury compared with the control group (P <0.01). CONCLUSION: Endogenous nitric oxide can protect gastric mucosal injury induced by stress and inhibit or promote its synthesis, which may aggravate or alleviate mucosal injury. This effect is achieved by affecting mucosal blood flow.