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目的探讨糖皮质激素和氨基胍对大潮气量机械通气大鼠肺组织诱导型一氧化氮合酶(iNOS)及一氧化氮(NO)的干预作用。方法32只雄性Wistar大鼠随机分为对照组、大潮气量组、地塞米松(DXM)组和氨基胍(AG)组。用反转录-聚合酶链反应(RT-PCR)法检测肺组织iNOS mRNA表达,用SABC免疫组织化学染色法检测肺组织iNOS蛋白表达,用硝酸还原酶法测定肺组织和血浆NO含量。结果与对照组相比,各实验组肺组织iNOS mRNA及其蛋白表达水平、肺组织和血浆NO含量均明显升高(P均<0.01);与大潮气量组相比,DXM组和AG组肺组织iNOS mRNA及其蛋白表达水平、肺组织和血浆NO含量均明显降低(P均<0.01),但DXM组和AG组比较差异无统计学意义(P>0.05)。结论糖皮质激素和氨基胍可通过抑制肺组织iNOS的表达,减少NO的生成,对大潮气量机械通气大鼠肺组织具有保护作用。
Objective To investigate the effects of glucocorticoid and aminoguanidine on inducible nitric oxide synthase (iNOS) and nitric oxide (NO) in lung tissue of rats with large tidal volume ventilation. Methods Thirty-two male Wistar rats were randomly divided into control group, high tidal volume group, DXM group and aminoguanidine group. The expression of iNOS mRNA in lung tissue was detected by reverse transcription-polymerase chain reaction (RT-PCR). The expression of iNOS protein in lung tissue was detected by SABC immunohistochemical method. The content of NO in lung tissue and plasma was determined by nitrate reductase method. Results Compared with the control group, the expression of iNOS mRNA and protein, the content of NO in lung tissue and plasma were significantly increased in all experimental groups (all P <0.01). Compared with the large tidal volume group, The expression of iNOS mRNA and protein, the contents of NO and NO in lung tissue and plasma were significantly decreased (all P <0.01), but there was no significant difference between DXM group and AG group (P> 0.05). Conclusion Glucocorticoid and aminoguanidine can protect the lung tissue of rats with large tidal volume of mechanical ventilation by inhibiting the expression of iNOS and reducing the production of NO.