Effect of endotoxin on systemic and skeletal muscle O2 extraction.

Effect of endotoxin on systemic and skeletal muscle O2 extraction.
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内毒素对全身和骨骼肌 O2 提取的影响。

DOI:
10.1152/jappl.1988.65.3.1377
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发表时间:
1988
期刊:
Journal of applied physiology (Bethesda, Md. : 1985)
影响因子:
--
通讯作者:
Schumacker,PT
Schumacker,PT
中科院分区:
--
文献类型:
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作者:
Samsel,RW;Nelson,DP;Sanders,WM;Wood,LD;Schumacker,PT

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成人呼吸窘迫综合征 (ARDS) 患者表现出 O2 消耗 (VO2) 对 O2 输送的病理依赖性(QO2,血流量 X 动脉 O2 含量)。在这些患者中,组织从血液中提取 O2 的能力存在缺陷,即使 QO2 正常,也可能导致组织对 O2 的需求得不到满足。内毒素管理在狗身上产生类似的状态,我们使用这个模型来研究可能有助于人类病理学的机制。我们测量了全身和后肢的 VO2 和 QO2,同时通过抽血减少心输出量。供应依赖开始时,内毒素组的全身 QO2 为 11.4 +/- 2.7 ml.kg-1.min-1,而对照组为 8.0 +/- 0.7(P 小于 0.05)。此时,内毒素处理的动物仅提取了 61 +/- 11% 的动脉 O2,而对照动物提取了 70 +/- 7%(P 小于 0.05)。内毒素治疗后全身摄氧量上升 15%(P 小于 0.05),但对照组没有变化。尽管内毒素处理的狗提取氧气的全身能力较差,但内毒素处理的狗和对照狗在供应依赖开始时分离的后肢提取氧气是相同的。在 QO2 正常水平下,内毒素治疗犬的后肢 VO2 比对照组高 23%(P 小于 0.05)。对照组和内毒素治疗犬之间骨骼肌血流量没有差异。因此,在内毒素血症中骨骼肌没有过度灌注,也不会通过窃取其他组织的血流而导致全身性提取缺陷。经过内毒素处理的狗的骨骼肌显示出摄氧量增加,但氧气提取没有缺陷,这两个方面都与肠道不同。
Patients with the adult respiratory distress syndrome (ARDS) show a pathological dependence of O2 consumption (VO2) on O2 delivery (QO2, blood flow X arterial O2 content). In these patients, a defect in tissues' ability to extract O2 from blood can leave tissue O2 needs unmet, even at a normal QO2. Endotoxin administration produces a similar state in dogs, and we used this model to study mechanisms that may contribute to human pathology. We measured systemic and hindlimb VO2 and QO2 while reducing cardiac output by blood withdrawal. At the onset of supply dependence, the systemic QO2 was 11.4 +/- 2.7 ml.kg-1.min-1 in the endotoxin group vs. 8.0 +/- 0.7 in controls (P less than 0.05). At this point, the endotoxin-treated animals extracted only 61 +/- 11% of the arterial O2, whereas control animals extracted 70 +/- 7% (P less than 0.05). Systemic VO2 rose by 15% after endotoxin (P less than 0.05) but did not change in controls. Despite this poorer systemic ability to extract O2 by the endotoxin-treated dogs, isolated hindlimb O2 extraction at the onset of supply dependence was the same in endotoxin-treated and control dogs. At normal levels of QO2, hindlimb VO2 in endotoxin-treated dogs was 23% higher than in controls (P less than 0.05). Fractional blood flow to skeletal muscle did not differ between control and endotoxin-treated dogs. Thus skeletal muscle was not overperfused in endotoxemia and did not contribute to a systemic extraction defect by stealing blood flow from other tissues. Skeletal muscle in endotoxin-treated dogs demonstrated an increase in VO2 but no defect in O2 extraction, differing in both respects from the intestine.