肌肉Na+K+ATPase活性与败血症休克时乳酸度升高之间的关系:一项前性研究
Bruno Levy1, Sébastien Gibot, Patricia Franck
1Service de Réanimation Médicale, Hôpital Central, 54035 Nancy, France. b.levy@chu-nancy.fr
Lancet (London, England)
|March 9, 2005
概括
在败血症休克中,骨肌肉通过Na+K+ ATPase刺激以有氧方式产生乳酸,而不仅仅来自缺氧. 抑制这种酶减少了肌肉乳酸,表明乳酸是一种疾病标志物,而不仅仅是氧气欠缺指标.
科学领域:
- 生物化学 生物化学
- 生理学 生理学 生理学
- 临界护理医学 临界护理医学
背景情况:
- 败血性休克中的高乳酸血常常被错误地归因于组织缺氧.
- 这种情况并非始终与 perfusion 指标相关,也不是通过增加氧气输送来改善的.
- 骨肌肉可以以有氧方式产生乳酸,这与Na+K+ ATPase活性有关.
研究的目的:
- 调查抑制Na+K+ ATPase是否可以降低败血症休克患者的肌肉乳酸生产.
主要方法:
- 在14名败血性休克患者中,微透析探头被插入四头肌肌.
- 探头注入了ouabain (Na+K+ ATPase 抑制剂) 或林格溶液.
- 在透析液和动脉血液中测量了乳酸盐和酸盐度.
主要成果:
- 患者表现出血中乳糖水平升高 (平均值为4.0mmol/L).
- 肌肉中的乳酸盐和酸盐水平明显高于动脉水平.
- 输入Ouabain有效地阻止了肌肉的乳酸盐和酸盐生产 (p=0.0001).
结论:
- 由Na + K + ATPase刺激的骨肌肉是通过有氧糖解通过败血症休克中重要的乳酸源.
- 在败血症休克中,乳酸盐度意味着疾病的严重程度和不良结果,不一定是缺氧.
- 乳酸盐应该被视为一种代谢信号,其清除可能是一个有价值的复苏终点.
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