Hussain S N
Department of Medicine, Royal Victoria Hospital, McGill University, Montreal, Quebec, Canada.
Mol Cell Biochem. 1998 Feb;179(1-2):125-34. doi: 10.1023/a:1006864021783.
It became evident in the past 12 years that venitlatory muscle contractile performance is significantly impaired during the course of septic shock. In animal models of septic shock, depression of ventilatory muscle contractile performance has been shown to cause hypercapneic ventilatory failure and respiratory arrest. Failure of ventilatory muscle contractility in septic shock has never been attributed to a single factor, but two groups of factors are likely to be involved: (a) increased ventilatory muscle metabolic demands due to augmentation of ventilation, hypoxemia and increased pulmonary impedance; and (b) specific cellular, metabolic, immune and hemodynamic defects which interfere with several processes necessary for normal force generation. These defects are mediated by complex interactions between several local and systematic mediator such a bacterial endotoxin, proinflammatory cytokines, prostaglandins, platelet activating factor, reactive oxygen species and nitric oxide. This is a summary of how these interactions are likely to interfere with ventilatory muscle contractile performance in septic shock with particular emphasis on the newly described role of nitric oxide.
在过去12年中已明确，在脓毒性休克病程中，通气肌的收缩性能会显著受损。在脓毒性休克的动物模型中，通气肌收缩性能的降低已被证明会导致高碳酸血症性通气衰竭和呼吸骤停。脓毒性休克中通气肌收缩力的衰竭从未归因于单一因素，但可能涉及两组因素：(a) 由于通气增加、低氧血症和肺阻抗增加导致通气肌代谢需求增加；(b) 特定的细胞、代谢、免疫和血流动力学缺陷，这些缺陷会干扰正常力量产生所需的几个过程。这些缺陷是由几种局部和全身介质（如细菌内毒素、促炎细胞因子、前列腺素、血小板活化因子、活性氧和一氧化氮）之间的复杂相互作用介导的。这是关于这些相互作用可能如何干扰脓毒性休克中通气肌收缩性能的综述，特别强调了一氧化氮新描述的作用。
