内源性NO对应激性胃粘膜损伤保护作用的实验研究

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）反映粘膜损伤程度,Ｇｒｅｓｓ法检测血浆及粘膜ＮＯ含量,ＬＤＦ－３型激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可致严生的胃粘膜损伤,同时粘膜血流量明显下降,

Experimental study on the protective effect of endogenous NO on stress-induced gastric mucosal lesions

Objective: To study the role of endogenous NO in protecting gastric mucosa from stress induced injury and its mechanism. Methods: Acute gastric mucosal damage was induced by exposing SD rats to water immersion and restraint stress (WRS) for 4 h. The extent of gastric mucosal lesions was evaluated by ulcer index (UI). NO contents in plasma and mucosa were measured by means of Griess reaction and GMBF was monitored by using LDF 3 Flowmetry. L NAME and L Arg were used to inhibit or promote the synthesis of endogenous NO to examine their effects on GMBF, NO contents and mucosal injuries. Results: Small round or linear haemorrhagic erosions were induced in the oxyntic glandular area after rats exposed to WRS. Meanwhile, GMBF decreased and NO contents in plasma and gastric mucosa increased significangly compared with those without WRS. L NAME not only further decreased GMBF and inhibited the increases of NO contents but also aggravated the extent of gastric mucosal lesions. In contrast, L Arg increased both GMBF and NO contents resulting in the lessening of mucosal injuries. All these changes were significant compared with control group. Conclusion: Endogenous NO plays an important role in preventing stress induced acute gastric mucosal lesions by regulating GMBF. Inhibition or promotion of its synthesis can significantly exacerbate or mitigate acute gastric mucosal injuries.