内皮素，一氧化氮在内毒素血症大鼠胃粘膜损伤中的作用

目的：观察内皮素－1（ET－1）、一氧化氮（NO）在内毒素血症胃粘膜扣伤中的作用。方法：应用内毒素血症胃粘膜损伤模型分别观察血浆、胃粘膜中ET－1、NO含量变化，以及胃粘膜血流（GMBF）、胃粘膜损伤面积的变化。结果：内毒素血症时ET－1含量增加、NO含量减少，特异性内皮素受体ETAR阻滞剂（BQ123）、NO前体L－精氨酸（L－Arg）能减轻内毒素血症时胃粘膜损伤的程度。一氧化氮合酶阻滞剂N^G－硝基－L－精氨酸甲酯（L－NAME）加重了该模型胃粘膜的损伤。结论：内源性ET－1／NO失衡参与了内毒素血症时胃粘膜损伤病理过程。纠正内源性ET－1／NO失衡，通过改善了GMBF，减轻胃粘膜损伤。

Role of endothelin-1 and nitric oxide in endotoxemia-induced gastric mucosal injury in rats

Aim To study the effects of endothelin 1(ET 1) and Nitric Oxide(NO) in endotoxemia induced gastric mucosal injury.Methods The changes of ET 1 and NO in the levels of plasma and mucosal were observed in endotoxemia model of rats.Gastric mucosal blood flow (GMBF) and mucosal lesions were also studied.Results Both plasma and mucosal ET 1 significantly increased in endotoxemia rats compared with the control values.BQ 123 ,an endothelin A receptor antagonist could partially alleviate the gastric mucosal injury.So did L Arg,the physological NO precureor.While NO synthase inhibitor N G nitro L arginine exaggerate the gastric mucosal injury.Conclusion The imbalance of endogenous ET 1/NO proportion plays an important role in the pathogenesis of endotoxemia induced gastric mucosal damage through impairment of mucosal microcirculation.Further,endothelin A antagoinsts may have therapeutic benefits for endotoxemia induced gastric mucosal damage through improve GMBF.