Takada Y, Shimahara Y, Yamaguchi T, Nishizawa F, Mori K, Yamaoka Y, Ozawa K
Second Department of Surgery, Faculty of Medicine, Kyoto University, Japan.
Circ Shock. 1992 Oct;38(2):130-7.
To investigate whether or not platelet-activating factor (PAF) is a mediator of the liver injury resulting from transient hepatic inflow occlusion (Pringle's maneuver), the effect of pretreatment with a potent PAF antagonist (CV6209) on hepatic energy metabolism was evaluated following 30 min of inflow occlusion in rabbits. At 60 min after declamping, the arterial ketone body ratio (AKBR; acetoacetate/3-hydroxybutyrate), reflecting hepatic mitochondrial redox state (NAD+/NADH), increased to 1.10 +/- 0.05 (mean +/- SEM) in the CV6209 (5 mg/kg)-pretreated group (group 1, n = 5) compared with 0.72 +/- 0.06 (P less than 0.01) in the untreated group (group 2, n = 5). Hepatic energy charge at 60 min after declamping was significantly higher in group 1 than in group 2 (0.871 +/- 0.010 vs. 0.800 +/- 0.023; P less than 0.05). Pretreatment with CV6209 had no significant influence on these parameters in sham-operated animals. The present study demonstrates that pretreatment with CV6209 has a protective effect against the impairment of hepatic energy metabolism following transient hepatic inflow occlusion.
为了研究血小板活化因子（PAF）是否是短暂性肝血流阻断（Pringle手法）所致肝损伤的介质，在兔肝血流阻断30分钟后，评估了用强效PAF拮抗剂（CV6209）预处理对肝能量代谢的影响。在松开阻断钳60分钟后，反映肝线粒体氧化还原状态（NAD+/NADH）的动脉酮体比率（AKBR；乙酰乙酸/3-羟基丁酸）在CV6209（5mg/kg）预处理组（第1组，n = 5）中升至1.10±0.05（平均值±标准误），而未处理组（第2组，n = 5）中为0.72±0.06（P<0.01）。松开阻断钳60分钟后的肝能量负荷在第1组显著高于第2组（0.871±0.010对0.800±0.023；P<0.05）。在假手术动物中，CV6209预处理对这些参数无显著影响。本研究表明，CV6209预处理对短暂性肝血流阻断后肝能量代谢的损害具有保护作用。
