REEVALUATION OF THE ROLE OF CELLULAR HYPOXIA AND BIOENERGETIC FAILURE IN SEPSIS
REEVALUATION OF THE ROLE OF CELLULAR HYPOXIA AND BIOENERGETIC FAILURE IN SEPSIS
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DOI：
10.1001/jama.267.11.1503
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发表时间：
1992-03-18
影响因子：
120.7
通讯作者：
KARL, IE
中科院分区：
文献类型：
--
作者：
HOTCHKISS, RS;KARL, IE
脓毒症通常以一系列代谢异常为特征：血浆乳酸浓度升高，代谢性酸中毒，糖酵解增加，以及异常的“分娩依赖性”耗氧量。有两种假说可以解释这些代谢异常：(1)由微循环血流异常引起的细胞缺氧；(2)细胞产生能量代谢途径的缺陷。我们对大鼠肌肉、肝脏、心脏、大脑和血浆的研究结果表明，在这些败血症组织中没有生物能量衰竭的证据，乳酸生成的增加并不一定是由于细胞缺氧。利用体内磷31核磁共振波谱、[F-18]氟咪唑和微荧光酶技术验证了细胞氧合和生物能量的充足性。这些研究的结果以及一些临床调查的结果表明，这两种假设都不能充分解释败血症的典型代谢特征，败血症的病理生理学有待进一步阐明。本文讨论了这些研究及其重要的临床意义。
Sepsis is frequently characterized by a number of metabolic abnormalities: increased plasma lactate concentration, metabolic acidosis, increased glycolysis, and an abnormal "delivery-dependent" oxygen consumption. Two hypotheses have been advanced to explain these metabolic abnormalities: (1) cellular hypoxia resulting from abnormal microcirculatory blood flow or (2) defect(s) in energy-producing metabolic pathways of cells. Results of our studies on rat muscle, liver, heart, brain, and plasma suggest that there is no evidence of bioenergetic failure in these septic tissues and that the increase in lactate production is not necessarily due to cellular hypoxia. The adequacy of cellular oxygenation and bioenergetics was verified using in vivo phosphorus 31 nuclear magnetic resonance spectroscopy, [F-18]fluoromisonidazole, and microfluorometric enzymatic techniques. Findings from these studies as well as results from several clinical investigations indicate that neither hypothesis can adequately account for the metabolic features typical of sepsis and that the pathophysiology of sepsis awaits further clarification. These studies and important clinical implications are discussed.