Schirmer W J, Schirmer J M, Naff G B, Fry D E
Department of Surgery, Veterans Administration Medical Center, Cleveland, OH 44106.
J Trauma. 1988 Sep;28(9):1295-300. doi: 10.1097/00005373-198809000-00001.
This study examines the effects of complement activation and of complement-induced oxygen radical production on the principal determinant of hepatic function, i.e., effective hepatic blood flow (EHBF). Female Sprague-Dawley rats received cobra venom factor, 40 units/kg, in two divided doses at 30-minute intervals. At t = 2 hours, thermodilution cardiac output, mean arterial pressure, heart rate, hematocrit, and EHBF by galactose clearance were determined. Complement activation produced a significant depression in EHBF independent of changes in systemic perfusion. To determine whether oxygen radicals participated in the insult, additional animals were pretreated with superoxide dismutase, 6 mg/kg, plus catalase, 15 mg/kg, immediately before complement activation. Concomitant treatment with the oxygen radical scavengers attenuated the degree of complement-induced hepatic ischemia, again independent of effects on systemic perfusion. This study suggests that the reduction in hepatic blood flow that accompanies animal models of trauma and sepsis may result, in part, from the sequelae of complement activation with oxygen radicals as secondary mediators.
本研究考察补体激活及补体诱导的氧自由基生成对肝功能的主要决定因素即有效肝血流量（EHBF）的影响。雌性Sprague-Dawley大鼠按40单位/千克的剂量分两次、间隔30分钟注射眼镜蛇毒因子。在t = 2小时时，通过热稀释法测定心输出量、平均动脉压、心率、血细胞比容，并通过半乳糖清除率测定EHBF。补体激活导致EHBF显著降低，且与全身灌注的变化无关。为确定氧自由基是否参与了这种损害，在补体激活前立即给另外的动物预先注射6毫克/千克的超氧化物歧化酶加15毫克/千克的过氧化氢酶。氧自由基清除剂的联合治疗减轻了补体诱导的肝缺血程度，同样与对全身灌注的影响无关。本研究提示，创伤和脓毒症动物模型中伴随的肝血流量减少可能部分是由于补体激活的后遗症，氧自由基作为继发性介质参与其中。
