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本文着重论述器官功能衰竭(MOF)病人的氧化代谢问题,氧化代谢的缺乏可能是形成MOF的关键问题。仅观察败血病MOF病人,就能发现氧化代谢明显缺乏,即病人的心输出量有特征性增加而不是下降。病人的周围血管阻力下降、全身氧耗量的增加可能超过了基础状态,但动静脉氧含量的差别极小。即使心肌过度收缩以加快血液循环,乳酸酸中毒将出现在低血压形成之前。当然,此时多个器官系统已受累。许多体液介质可能参与形成MOF的代谢及其它过程。如:细胞间素-1、类花生酸、鸦
This article focuses on the oxidative metabolism in patients with organ failure (MOF). The lack of oxidative metabolism may be the key issue for the formation of MOF. Only observing sepsis MOF patients, we can find a clear lack of oxidative metabolism, that is, the patient’s cardiac output has a characteristic increase rather than decline. Patients with decreased peripheral vascular resistance, systemic oxygen consumption may increase more than the basic state, but very little difference between the arterial and venous oxygen content. Even if the myocardium contracts excessively to speed up blood circulation, lactic acidosis will occur before hypotension develops. Of course, multiple organ systems have been involved. Many bodily fluids may be involved in the metabolism of MOF formation and other processes. Such as: Cytosin-1, eicosanoid, crow