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一氧化氮、心肌衰竭与脓毒性休克

Nitric oxide, myocardial failure and septic shock.

作者信息

Brady A J

机构信息

Department of Cardiology, Queen Elizabeth Hospital, Birmingham, UK.

出版信息

Int J Cardiol. 1995 Jul;50(3):269-72. doi: 10.1016/0167-5273(95)02387-c.

Abstract

Septic shock is a major cause of hospital deaths despite modern intensive therapy. Profound hypotension is caused by a collapse of regulatory mechanisms. Recent advances have established that bacterial products and the host inflammatory response together generate uncontrolled production of nitric oxide throughout the vasculature, accounting for this vasodilatation. Progressive heart failure is a further manifestation of established septic shock. Emerging research suggests that overproduction of nitric oxide within the myocardium likewise leads to loss of normal myocardial function. The possibility exists that exciting future therapies will be able to selectively inhibit the overproduction of nitric oxide and aid recovery from this frequently lethal condition.

摘要

尽管有现代强化治疗手段,感染性休克仍是医院死亡的主要原因。严重的低血压是由调节机制崩溃引起的。最近的研究进展表明,细菌产物和宿主炎症反应共同导致整个血管系统中一氧化氮的失控产生,这就是血管扩张的原因。进行性心力衰竭是已确诊的感染性休克的进一步表现。新出现的研究表明,心肌内一氧化氮的过度产生同样会导致正常心肌功能丧失。未来有可能开发出令人兴奋的治疗方法,能够选择性地抑制一氧化氮的过度产生,并帮助患者从这种常常致命的疾病中康复。

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