Hotchkiss R S, Rust R S, Dence C S, Wasserman T H, Song S K, Hwang D R, Karl I E, Welch M J
Department of Anesthesiology, Washington University School of Medicine, St. Louis, Missouri 63110.
Am J Physiol. 1991 Oct;261(4 Pt 2):R965-72. doi: 10.1152/ajpregu.1991.261.4.R965.
Underlying cellular hypoxia, which may be difficult to detect, has been postulated to be a major cause of morbidity and mortality in sepsis. We employed the novel hypoxic marker [18F]fluoromisonidazole to determine whether cellular hypoxia was present in a peritonitis model of sepsis in the rat. A second group of septic and control rats had organ blood flow measurements determined by the radiolabeled microsphere technique to relate possible ischemia to decreased organ perfusion. No evidence of cellular hypoxia was detected in skeletal muscle, brain, liver, heart, or diaphragm in the septic rats. Ligation of the femoral artery caused a greater reduction in flow (55% decrease vs. 20% decrease, P less than 0.05) and an increased retention of [18F]fluoromisonidazole in skeletal muscle of the septic rats. We conclude that sepsis does not invariably result in systemic, i.e., multiorgan, cellular hypoxia and that underlying cellular hypoxia is not the major pathophysiological abnormality in sepsis. The greater reduction in muscle blood flow and the increased retention of [18F]fluoromisonidazole in the ischemic muscle of septic rats implies that they may be more vulnerable to hypoxia.
潜在的细胞缺氧可能难以检测，据推测是脓毒症发病和死亡的主要原因。我们采用新型缺氧标志物[18F]氟米索硝唑来确定大鼠脓毒症腹膜炎模型中是否存在细胞缺氧。第二组脓毒症大鼠和对照大鼠通过放射性微球技术测定器官血流，以关联可能的缺血与器官灌注减少情况。在脓毒症大鼠的骨骼肌、脑、肝、心脏或膈肌中未检测到细胞缺氧的证据。结扎股动脉导致脓毒症大鼠骨骼肌血流减少幅度更大（减少55% 对比减少20%，P<0.05），且[18F]氟米索硝唑在骨骼肌中的滞留增加。我们得出结论，脓毒症并不总是导致全身性即多器官细胞缺氧，且潜在的细胞缺氧不是脓毒症的主要病理生理异常。脓毒症大鼠缺血肌肉中肌肉血流减少幅度更大以及[18F]氟米索硝唑滞留增加表明它们可能更易发生缺氧。
