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组织缺氧在大肠杆菌内毒素血症期间作为乳酸酸中毒机制的作用。

Role of tissue hypoxia as the mechanism of lactic acidosis during E. coli endotoxemia.

作者信息

Hurtado F J, Gutierrez A M, Silva N, Fernandez E, Khan A E, Gutierrez G

机构信息

Pulmonary and Critical Care Medicine Division, University of Texas, Houston 77030.

出版信息

J Appl Physiol (1985). 1992 May;72(5):1895-901. doi: 10.1152/jappl.1992.72.5.1895.

DOI:10.1152/jappl.1992.72.5.1895
PMID:1601797
Abstract

We compared the hemodynamic and metabolic alterations produced in rabbits by similar decreases in cardiac output created by inflating a balloon placed in the right ventricle (n = 6) with those produced by an intravenous bolus of Escherichia coli lipopolysaccharide (LPS; SEP group; n = 6). We measured O2 consumption (VO2), O2 transport (TO2), and O2 extraction ratio (ERO2) for the whole animal and also for the left hindlimb. Both groups experienced similar decreases in cardiac output, systemic TO2, and VO2 and similar increases in ERO2. For the hindlimb, TO2 was similar, but VO2 and ERO2 were lower for the SEP group 30 min after LPS administration (P less than 0.05); however, this difference disappeared during the remainder of the experiment. Arterial lactate concentration was greater (P less than 0.05) for the SEP group. There were no differences in skeletal muscle PO2, measured with a multiwire surface electrode, or in cardiac and skeletal muscle concentrations of high-energy phosphates. We hypothesize that a direct effect of LPS on cellular metabolism may have resulted in greater arterial lactate concentration for the SEP group.

摘要

我们比较了通过向置于右心室的气球充气(n = 6)使家兔心输出量产生类似降低所引起的血流动力学和代谢改变,以及静脉注射大肠杆菌脂多糖(LPS;脓毒症组;n = 6)所产生的血流动力学和代谢改变。我们测量了全动物以及左后肢的氧消耗(VO2)、氧运输(TO2)和氧摄取率(ERO2)。两组的心输出量、全身TO2和VO2均出现类似程度的降低,ERO2均出现类似程度的升高。对于后肢,LPS给药30分钟后脓毒症组的TO2相似,但VO2和ERO2较低(P < 0.05);然而,在实验的其余时间里这种差异消失。脓毒症组的动脉乳酸浓度更高(P < 0.05)。使用多线表面电极测量的骨骼肌PO2,以及心脏和骨骼肌中的高能磷酸盐浓度均无差异。我们推测,LPS对细胞代谢的直接作用可能导致脓毒症组的动脉乳酸浓度更高。

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