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The Relationship of Ventricular Dynamics and Mitochondrial Nitric Oxide Synthase Activity in Septic Shock Models

机译:心室动力学和线粒体一氧化氮合成酶活性在脓毒休克模型中的关系

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The aim of the present study was to investigate the role of mitochondrial nitric oxide synthase (mtNOS) in the septic shock and analyze its relationship to ventricular contractility. Two models of septic shock [lipopolysaccharide (LPS)-induced and cecal ligation and puncture (CLP)-induced] were used. There was a significant depression of ventricular contractile parameters recorded in the late stage of the septic shock. After measurement of ventricular-dynamic parameters, mitochondrial and cytoplasmic fractions were isolated and their nitric oxide synthase (NOS) activity was assessed using a NOS activity assay kit. Both models showed a larger increase in mitochondrial NOS activity than that in cytosol. However, the increase in mtNOS activity in the LPS-induced shock model was less pronounced than in the CLP-induced model. Regression analysis shows that mitochondrial nitric oxide sunthase (mtNOS) activity is negatively correlative to the left ventricular developed pressure in CLP model. The results suggest that mitochondrial NOS may mainly contribute to the ventricular depression in the septic shock.
机译:本研究的目的是探讨线粒体一氧化氮合酶(MTNO)在脓毒症休克中的作用,并分析其与心室收缩性的关系。使用了两种脓毒症休克[脂多糖(LPS) - 诱导和盲肠连接和穿刺(CLP)诱导]。在化粪池休克后期记录的心室收缩参数存在显着抑郁症。在测量心室动度参数后,分离线粒体和细胞质级分,并使用NOS活性测定试剂盒评估其一氧化氮合酶(NOS)活性。两种模型显示出比细胞溶胶的线粒体NOS活性较大增加。然而,LPS引起的冲击模型中的MTNOS活性的增加比CLP诱导的模型更显着。回归分析表明,线粒体一氧化氮阳离子酶(MTNO)活性与CLP模型中的左心室发育压力负相关。结果表明,线粒体NoS可以主要有助于脓毒症休克的心室抑郁症。

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