乳酸是伤害或败血症组织缺氧的不可靠指标
J H James1, F A Luchette, F D McCarter
1Department of Surgery, University of Cincinnati Medical Center, OH, USA. jamesjh@ucmail.uc.edu
Lancet (London, England)
|August 28, 1999
概括
在创伤或败血症中血糖水平升高可能源于有氧糖解,而不仅仅是组织缺氧. 这挑战了假设高乳酸总是标志着 poor perfusion 的假设.
科学领域:
- 生物化学 生物化学
- 生理学 生理学 生理学
- 创伤和重症监护医学 创伤和重症监护医学
背景情况:
- 在创伤/败血症中高血糖 (超乳糖血症) 通常意味着组织缺氧和无氧糖解.
- 即使血液动力学和尿液输出正常时,这种假设仍然存在.
- 在氧气充足的组织中产生乳酸盐的机制尚未得到充分探索.
研究的目的:
- 在受伤患者中提出超乳糖血症的替代假设.
- 调查有氧糖解在乳酸生成中的作用.
- 挑战血中乳糖水平升高作为低 perfusion 的唯一指标的传统解释.
主要方法:
- 对细胞能量生产区的审查 (氧化与糖解).
- 检查上腺素在刺激Na+-K+活动中的作用.
- 低血与受伤患者的Na+,K+-ATPase活性之间的相关性.
- 假设有氧糖解作为乳酸源.
主要成果:
- 有氧糖解可以为Na+-K+提供ATP,由上腺素刺激.
- 增加的Na+,K+-ATPase活性,可能被低血糖症表明,可能会驱动有氧糖解.
- 这种机制解释了为什么超乳血症可能与输液指标无关或与氧气输送没有改善.
结论:
- 在创伤/败血症中血中乳酸水平升高可能反映了由于上腺素刺激的Na+-K+活动而导致骨肌中的有氧糖解增加.
- 这与传统的乳酸盐看法形成鲜明对比,它仅仅表明来自低的无氧糖解.
- 仅仅依靠高乳酸进行复苏,可能会导致不必要的干预,如输血和内.
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