Fukuoka T
First Department of Surgery, Nara Medical University, Kashihara, Japan.
Nihon Geka Gakkai Zasshi. 1990 Oct;91(10):1596-602.
The potential effect of CV6209, a platelet activating factor (PAF) antagonist, on shock after temporary hepatic inflow occlusion was investigated. Five groups of rats were given following chemicals i.v. (Group A: both 3 mg/kg of CV6209 and 100 U/kg of heparin, Group B: 3 mg/kg of CV6209, Group C: 100 U/kg of heparin, Group D: 4 ml/kg of normal saline, Group E: 4 ml/kg of normal saline under splanchnic decompression with port-jugular bypass) and were subjected to 45 minutes of hepatic inflow occlusion. The survival rates 24 hours after the occlusion were 80%, 60% 45%, 30% and 80% in groups A, B, C, D and E, respectively. All rats except for those in group E developed hypotension during the occlusion period. The blood pressure was reversed to pre-occlusion level after declamping in groups A and B, although hypotension continued in groups C and D. Blood chemistry also revealed diminished elevation of serum mitochondrial GOT after the occlusion in PAF antagonist group. These results suggest that portal congestion is the most responsible for shock and death after temporary hepatic inflow occlusion and PAF is a mediator of the injury.
研究了血小板活化因子（PAF）拮抗剂CV6209对暂时性肝血流阻断后休克的潜在影响。将五组大鼠静脉注射下列化学物质（A组：3mg/kg的CV6209和100U/kg的肝素；B组：3mg/kg的CV6209；C组：100U/kg的肝素；D组：4ml/kg的生理盐水；E组：在门静脉-颈静脉旁路内脏减压下注射4ml/kg的生理盐水），并进行45分钟的肝血流阻断。阻断后24小时的存活率在A、B、C、D和E组中分别为80%、60%、45%、30%和80%。除E组外，所有大鼠在阻断期间均出现低血压。A组和B组在松开夹闭后血压恢复到阻断前水平，而C组和D组低血压持续存在。血液化学分析还显示，PAF拮抗剂组在阻断后血清线粒体谷草转氨酶升高幅度减小。这些结果表明，门静脉淤血是暂时性肝血流阻断后休克和死亡的最主要原因，PAF是损伤的介质。
