Lelli J L, Drongowski R A, Gastman B, Remick D G, Coran A G
Section of Pediatric Surgery, C.S. Mott Children's Hospital, Ann Arbor, Michigan.
Circ Shock. 1993 Mar;39(3):178-87.
Coenzyme Q10 (CoQ) has been promoted as an effective agent for reducing the deleterious effects of septic shock by acting as an oxygen free radical scavenger and thus stabilizing mitochondrial membranes and by inhibiting the arachidonic acid metabolic pathway and the formation of various prostaglandins. This study was undertaken to evaluate the effect of CoQ in a live Escherichia coli model of canine septic shock. Group I (E. coli, n = 5) animals received an LD100 dose of 10(9) live E. coli/kg and were given no further treatment. Group II (CoQ, n = 5) animals received a 20-mg/kg bolus of CoQ without further treatment. Group III (CoQ + E. coli, n = 5) animals received a 20-mg/kg bolus of CoQ 10 min prior to a bacterial infusion as in group 1. Mean arterial pressure stabilized at 70% of baseline levels (P < .002), while cardiac output remained near 50% of baseline levels (P < .053) in group III compared to group I dogs. The arachidonic acid metabolites, prostaglandin E2, Thromboxane B2, and leukotriene B4 were significantly elevated in groups I and III (vs. group II) (P < 0.05). The catecholamines, tumor necrosis factor (TNF) and interleukin 6 (IL-6) were significantly elevated in groups I and III (vs. group II) (P < 0.05). Fluorescent products (lipid peroxidation activity) were elevated in group I (vs. groups II and III) at 120 and 180 min (P < 0.05). We conclude that CoQ supports cardiovascular hemodynamics and prevents free radical mediated lipid peroxidation during live E. coli septic shock, and its effect is not due to altered levels of humoral or cytokine mediators.
辅酶Q10（CoQ）已被宣传为一种有效药物，可通过作为氧自由基清除剂来减少脓毒性休克的有害影响，从而稳定线粒体膜，并通过抑制花生四烯酸代谢途径和各种前列腺素的形成来发挥作用。本研究旨在评估CoQ在犬脓毒性休克的活大肠杆菌模型中的作用。第一组（大肠杆菌组，n = 5）动物接受10⁹活大肠杆菌/kg的LD100剂量，且未接受进一步治疗。第二组（CoQ组，n = 5）动物接受20 mg/kg的CoQ推注，未进行进一步治疗。第三组（CoQ +大肠杆菌组，n = 5）动物在细菌注入前10分钟接受20 mg/kg的CoQ推注，方式同第一组。与第一组犬相比，第三组的平均动脉压稳定在基线水平的70%（P <.002），而心输出量保持在基线水平的近50%（P <.053）。第一组和第三组（与第二组相比）的花生四烯酸代谢产物、前列腺素E2、血栓素B2和白三烯B4显著升高（P < 0.05）。第一组和第三组（与第二组相比）的儿茶酚胺、肿瘤坏死因子（TNF）和白细胞介素6（IL-6）显著升高（P < 0.05）。第一组（与第二组和第三组相比）在120分钟和180分钟时荧光产物（脂质过氧化活性）升高（P < 0.05）。我们得出结论，CoQ在活大肠杆菌脓毒性休克期间支持心血管血液动力学并防止自由基介导的脂质过氧化，其作用并非由于体液或细胞因子介质水平的改变。
