门脉高压性胃病胃粘膜组织一氧化氮及过氧化脂质的改变

目的 探讨肝硬化门脉高压患者胃粘膜局部一氧化氮（NO）的生成，氧自由基及脂质过氧化反应与胃粘膜病变的关系。方法 测定19便肝硬化合并门脉高压性胃病（Portal hypertensive gastropathy,PHG）患者胃粘膜细胞中NO及丙二醛（MDA）水平，并与正常胃粘膜组织相对照，分析NO与MDA及肝功能损害程度的相关性。结果 HPG患者胃粘膜组织NO及MDA水平明显高于正常胃粘膜，其中重度PHG者增高更为明显；19例PHG患者胃粘膜NO水平与肝功能Child-Pugh积分呈明显正相关（r＝0．702，P＜0．01）；19例PHG患者胃粘膜组织中NO与MDA水平呈明显正相关（r＝0．637，P＜0．01）。结论 在肝硬化门脉高压PHG的发生机理中，病理性NO过度生成不仅可直接引起胃粘膜损伤，且NO通过促进局部氧自由基及脂质近氧化反应而加重胃粘膜损伤。肝功能损害程度与胃粘膜NO产生的量及粘膜病变的严重程度均有密切关系。

The changes of nitric oxide and malondialdehyde of gastric mucosa in patients with portal hypertensive gastropathy

Objective To study the relationship between nitric oxide (NO) or oxygen-derived free radical and pathogenesis of portal hypertensive gastropathy (PHG). Methods NO and malondialdehyde (MDA) of gastric mucosal tissue were measured in 19 patients with post hepatitis cirrhosis complicated by PHG. Results The NO and MDA contents of gastric mucosal tissue in the patients with PHG were significantly higher than those of normal control, the increase of the NO and MDA contents in the patients with severe PHG were much more significant. A strong positive correlation was found between NO contents of gastric mucosal tissue in 19 patients with PHG and Child-Pugh score ( r =0.702, P <0.01). Gastric mucosal tissue NO contents were correlated positively with MDA contents ( r =0.637, P <0.01). Conclusion The increase of nitric oxide and oxygen-derived free radical (MDA) in gastric mucosal tissue played an important role in the pathogenetic mechanism of PHG. NO can not only directly induce mucosal damage, but also promote gastic mucosal damage induced by Oxygen-derived free radical in the patients with portal hypertension.