不同潮气量机械通气对大鼠肺组织iNOS、NO的影响

Effect of different tidal volumes of mechanical ventilation on nitric oxide and inducible nitric oxide synthase in rats

目的探讨诱导型一氧化氮合酶(iNOS)及一氧化氮(NO)在不同潮气量机械通气致大鼠急性肺损伤(VILI)中的作用。方法24只雄性Wistar大鼠随机分为对照组、小潮气量组和大潮气量组,每组各8只。用SABC免疫组化染色法检测肺组织iNOS蛋白表达,用逆转录-聚合酶链反应(RT-PCR)法检测肺组织iNOS mRNA表达,用硝酸还原酶法测定肺组织和血浆NO含量。结果与对照组和小潮气量组相比,大潮气量组大鼠肺组织iNOS mRNA及其蛋白表达水平以及肺组织和血浆NO含量均明显增加(均P<0.01);而小潮气量组与对照组各项指标比较差异无统计学意义(P>0.05)。结论大潮气量机械通气可诱导肺组织iNOS mRNA及其蛋白高表达,产生大量内源性NO导致肺组织损伤,而小潮气量机械通气对正常肺组织无明显影响。

Objective To explore the roles of inducible nitric oxide synthase（iNCS）and nitric oxide（NO）in acute lung injury（ALI） induced by different tidal volumes of ventilation in rats. Methods Twenty-four male Wistar rats were randomly divided into three groups： control group, low tidal volume group, high tidal volume group（ n = 8 in each group）. The expression of iNOS in lung tissues was detected by immunohistochemistry and RT-PCR,and the concentrations of NO in plasma and lung tissue were calculated. Resuits Cornpared with control group and low tidal volume group, the expression of iNOS and NO level increased significantly in high tidal volume group（ P〈 0.01 ）. But there was no statistical differences between low tidal volume group and control group（ P 〉0.05）. Conclusion The over-expression of iNOS and the excessive production of NO may be involved in the pathogenesis of ALl induced by high tidal volume ventilation, but low tidal volume ventilation has no distinct effects on normal lung tissue.