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Bacterial DNA and RNA induce rat cardiac myocyte contraction depression in vitro.

机译:细菌DNA和RNA诱导大鼠心脏肌细胞收缩抑郁体外。

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摘要

Sepsis and septic shock, the systemic immunologic and pathophysiologic response to overwhelming infection, are associated with perturbation of a variety of metabolic cell pathways and with multiple organ failure (MOF) including cardiac depression. This depression has been attributed to the effect of several circulating and locally produced proinflammatory mediators. Recent data suggest that bacterial nucleic acids can produce profound systemic inflammatory responses characterized by circulatory shock in intact animals. In this study, bacterial DNA and RNA derived from pathogenic clinical S. aureus and E. coli isolates are shown to induce early concentration-dependent depression of maximum extent and peak velocity of contraction of electrically paced neonatal rat ventricular myocytes in culture. Significant but more modest depression was generated by a nonpathogenic E. coli isolate. Pretreatment with a DNase or RNase abrogated this effect. Further, synthetic, double-stranded RNA (dsRNA) also induced concentration-dependent depression of myocyte contraction, with the effect also being prevented by pretreatment with RNase. These data suggest that bacterial DNA and RNA may contribute to myocardial depression during bacterial sepsis and septic shock.
机译:脓毒症和脓毒性休克,系统性免疫压倒性的和病理生理的反应感染,与微扰的相关联各种细胞代谢途径和多器官功能衰竭(MOF)包括心脏抑郁症。几个循环和局部的效果产生了促炎介质。表明细菌核酸可以生产深刻的系统性炎症反应特点是循环冲击完好无损动物。来自临床金黄色葡萄球菌致病性和E。杆菌分离株诱导早期所示浓度最大的经济萧条收缩的程度和峰值速度电的新生儿鼠心室细胞在文化。抑郁症是由一个非病原的E。杆菌分离。废除这一效应。双链RNA (dsRNA)也诱导肌细胞浓度萧条收缩,影响也被阻止通过与核糖核酸酶预处理。细菌的DNA和RNA可能导致心肌在细菌性败血症和抑郁感染性休克

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