梗阻性黄疸大鼠血浆一氧化氮及胃黏膜内相关合酶的测定及意义

[目的]观察梗阻性黄胆应激大鼠血浆一氧化氮含量及胃黏膜内诱生型一氧化氮合酶的变化,探讨梗阻性黄疸致急性胃黏膜损伤的发病机制.[方法]制作Wistar大鼠梗阻性黄疸及应激模型,观察胃黏膜损伤指数、血浆一氧化氮含量、胃黏膜诱生型一氧化氮合酶及胃黏膜形态学变化情况.[结果]各组大鼠胃黏膜损伤指数与假手术组比较均有显著性差异;梗阻性黄疸组及黄疸应激组大鼠血浆一氧化氮浓度显著升高,黄疸应激组胃黏膜诱生型一氧化氮合酶含量显著升高;除假手术组外,其他各组大鼠胃黏膜均有不同程度的损伤,胃黏膜各层均可见诱生型一氧化氮合酶阳性细胞.[结论]发生梗阻性黄疸时胃黏膜损伤指数升高,血浆一氧化氮浓度及胃黏膜诱生型一氧化氮合酶含量的升高可作为诊断梗阻性黄疸致急性胃黏膜损伤的参考指标.

Experimental study on nitric oxide and induced nitricoxide synthase in plasma and gastric tissue of obstructive jaundice in rats

OBJECTIVE The changes of nitric oxide （NO） content in plasma and induced nitricoxide synthase （iNOS） in gastric mucosa was analyzed to explore the mechanism of acute lesion of gastric mucosa in obstructive jaundice of rats. METHODS The models of obstructive jaundice and obstructive jaundice with stress were established in Wistar rats, and it was investigated that the index of gastric mucosa injury, changes of plasma NO content, iNOS and pathologic changes in gastric mucosa. RESULTS Injury index of gastric mucosa were significant difference in each groups than in fake operation group, and the plasma NO content increased prominently in obstructive jaundice and obstructive jaundice with stress, the iNOS content in gastric mucosa increased obviously in obstructive jaundice with stress. Except for fake operation group, the gastric mucosa was injured with different degree in all other groups, and iNOS-positive cells were observed in whole gastric mucosa layers. CONCLUSION Increases of injury index of gastric mucosa, plasma NO content and expression of iNOS may be as reference index for acute lesion of gastric mucosa induced by obstructive jaundice in rats.