论文部分内容阅读
以慢性常压缺氧的方法复制了大鼠慢性缺氧性肺动脉高压模型,观察了川芎嗪(LTZ80mg·kg~(-1),iP)对慢性缺氧性肺动脉高压的预防作用及cGMP含量(血浆和肺小动脉)和肺组织一氧化氮合成酶(NOS)基因的mRNA表达之变化.结果表明,慢性缺氧大鼠肺动脉平均压明显升高,但cGMP含量明显降低,肺组织NOS基因mRNA表达明显减弱;cGMP含量与肺动脉平均压呈明显负相关;LTZ对正常大鼠肺动脉压、cGMP含量和肺组织NOS基因的mRNA表达无明显影响,但可使慢性缺氧大鼠上述指标逆转.结果提示慢性缺氧大鼠肺组织NOS基因mRNA表达降低是慢性缺氧性肺动脉高压发病的机制之一,而LTZ增强了慢性缺氧大鼠肺NOS基因mRNA的表达可能是其预防慢性缺氧性肺动脉高压发生的重要机制.
The chronic hypoxic pulmonary hypertension model was replicated by chronic atmospheric hypoxia. The effect of tetramethylpyrazine (LTZ80mg·kg -1, iP) on chronic hypoxic pulmonary hypertension and cGMP content were observed. Changes in mRNA Expression of Nitric Oxide Synthase (NOS) Gene in Plasma and Pulmonary Arterioles) and in Lung Tissue. The results showed that the mean pulmonary arterial pressure in chronically hypoxic rats increased significantly, but the cGMP content decreased significantly, and the NOS gene mRNA in lung tissue was decreased. Expression was significantly decreased; cGMP content was negatively correlated with pulmonary arterial mean pressure; LTZ had no significant effect on pulmonary arterial pressure, cGMP content, and NOS gene mRNA expression in normal rats, but it could reverse the above indicators in chronic hypoxic rats. It suggests that the decrease of NOS gene mRNA expression in the lungs of chronic hypoxic rats is one of the mechanisms of chronic hypoxic pulmonary hypertension. LTZ increases the expression of NOS mRNA in lungs of chronic hypoxic rats may be the prevention of chronic hypoxic pulmonary arteries The important mechanism of the occurrence of high pressure.