Puchstein C, Lessire H, Kleine R
Klinik für Anästhesiologie und operative Intensivmedizin, Marienhospital Herne, Ruhr-Universität Bochum.
Anasth Intensivther Notfallmed. 1989 Aug;24(4):199-205.
Multiple-system organ failure is associated with progressive defects of cellular metabolism involving several organ systems. The metabolic failure is caused by a neural-hormonal reaction to trauma and sepsis and by humoral mediators damaging cell metabolism. Involved are catabolic hormones like catecholamines, cortisol and glucagon as well as the humoral mediators interleukin and arachidonic acid metabolites. There is an increase in resting energy expenditure and a derangement of utilization and production of adenine nucleotides. Severe injury, sepsis and multiple-system organ failure are associated with a 30-40% decreased content of energy rich phosphates in different tissues. The low energy charge potential is caused by the inability to use nutritional substrates adequately. Relative clearance and oxidation of glucose will advance fatty infiltration of the liver. Clearance and oxidation of fat is normal or often increased. If illness is progredient fat utilization will be disturbed. Although protein synthesis is increased in critical ill patients, due to excessive proteolyses net protein loss occur. In preterminal patients the ability of the liver to synthetize protein decreases, concentrations of several free amino acids in plasma increase, while the clearance for amino acids decreases.
多系统器官衰竭与涉及多个器官系统的细胞代谢进行性缺陷相关。代谢衰竭是由对创伤和脓毒症的神经 - 激素反应以及损害细胞代谢的体液介质引起的。涉及的分解代谢激素如儿茶酚胺、皮质醇和胰高血糖素，以及体液介质白细胞介素和花生四烯酸代谢产物。静息能量消耗增加，腺嘌呤核苷酸的利用和产生紊乱。严重损伤、脓毒症和多系统器官衰竭与不同组织中富含能量的磷酸盐含量降低30 - 40%相关。低能量电荷电位是由于无法充分利用营养底物所致。葡萄糖的相对清除和氧化会促进肝脏的脂肪浸润。脂肪的清除和氧化正常或常常增加。如果病情进展，脂肪利用将受到干扰。尽管危重病患者的蛋白质合成增加，但由于过度的蛋白水解会出现净蛋白质丢失。在濒死患者中，肝脏合成蛋白质的能力下降，血浆中几种游离氨基酸的浓度增加，而氨基酸的清除率降低。
