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首页> 外文期刊>American Journal of Physiology >Endotoxin-induced skeletal muscle contractile dysfunction: contribution of nitric oxide synthases.
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Endotoxin-induced skeletal muscle contractile dysfunction: contribution of nitric oxide synthases.

机译：内毒素诱导的骨骼肌收缩功能障碍：一氧化氮合酶的贡献。

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The aims of this study were to assess the role of nitric oxide (NO) and the contribution of different NO synthase (NOS) isoforms in skeletal muscle contractile dysfunction in septic shock. Four groups of conscious rats were examined. Group 1 served as control; group 2, 3, and 4 were injected with Escherichia coli endotoxin [lipopolysaccharide (LPS), 20 mg/kg i.p.] and killed after 6, 12, and 24 h, respectively. Protein expression was assessed by immunoblotting and immunostaining. LPS injection elicited a transient expression of the inducible NOS isoform, which peaked 12 h after LPS injection and disappeared within 24 h. This expression coincided with a significant increase in nitrotyrosine formation (peroxynitrite foot-print). Muscle expression of the endothelial and neuronal NOS isoforms, by comparison, rose significantly and remained higher than control levels 24 h after LPS injection. In vitro measurement of muscle contractility 24 h after LPS injection showed that incubation with NOS inhibitor (S-methyliosothiourea) restored the decline in submaximal force generation, whereas maximal muscle force remained unaffected. We conclude that NO plays a significant role in muscle contractile dysfunction in septic animals and that increased NO production is due to induction of the inducible NOS isoform and upregulation of constitutive NOS isoforms.
机译：这项研究的目的是评估败血性休克的骨骼肌收缩功能障碍中一氧化氮（NO）的作用和不同NO合酶（NOS）亚型的作用。检查了四组清醒大鼠。第一组作为对照组;第2、3和4组分别注射大肠杆菌内毒素[脂多糖（LPS），20 mg / kg i.p.]，分别在6、12和24小时后杀死。通过免疫印迹和免疫染色评估蛋白质表达。 LPS注射引起可诱导的NOS亚型的瞬时表达，在LPS注射后12小时达到峰值，并在24小时内消失。该表达与硝基酪氨酸形成的显着增加（过亚硝酸盐足迹）相吻合。相比之下，LPS注射后24小时，内皮和神经元NOS亚型的肌肉表达显着上升，并仍高于对照水平。注射LPS后24 h的体外肌肉收缩力测量显示，与NOS抑制剂（S-methyliosothiourea）一起温育可恢复亚最大力产生的下降，而最大肌力仍不受影响。我们得出的结论是，NO在脓毒症动物的肌肉收缩功能障碍中起着重要作用，并且NO产生的增加是由于诱导型NOS亚型的诱导和本构NOS亚型的上调。

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