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目的 评价一氧化氮(NO)在肝肺综合征(HPS)发病机制中的作用。方法 复习相关文献,并作综述性报道。结果 实验研究和临床研究证实,NO在肝肺综合征发病机制中起着重要作用,主要表现为:①HPS时肺内NO生成增多;②HPS时肺内NOS活性增强。HPS时肺内内皮型NO合酶(eNOS)合成增多的原因,可能与肝硬化患者内皮素1水平增加与血管扩张有关;也可能与HPS患者体内代谢产物的蓄积有关。结论 肺内eNOS合成增多是HPS患者肺内NO生成增多的主要原因。NO生成增多后发挥其舒血管效应,使肺血管扩张,通气/血流比例失调,从而导致低氧血症。但有关eNOS合成增多的原因和其它细胞因子与NO生成增加间的关系尚未阐明,还需进一步研究。
Objective To evaluate the role of nitric oxide (NO) in the pathogenesis of hepatopulmonary syndrome (HPS). Methods Review the relevant literature, and make a comprehensive report. Results Experimental studies and clinical studies confirmed that NO plays an important role in the pathogenesis of hepatopulmonary syndrome. The main manifestations are as follows: (1) NO production increases in the lungs in HPS; (2) NOS activity increases in the lungs during HPS. The reason for the increase of endothelin-1 (NO) synthase (eNOS) synthesis in HPS may be related to the increase of endothelin-1 level and vasodilatation in patients with cirrhosis. It may also be related to the accumulation of metabolites in HPS patients. Conclusions Increased synthesis of eNOS in the lungs is the main reason for increased NO production in the lungs of HPS patients. Increased production of nitric oxide exerts its vasodilative effect, causing pulmonary vasodilation and imbalance of ventilation / blood flow leading to hypoxemia. However, the relationship between the increased synthesis of eNOS and the increase of other cytokines and NO production has not been elucidated yet and further study is needed.