Experimental Studies on Reperfusion Injury of the Liver in Dogs

本研究以成年杂种犬为研究对象，通过阻断肝血流及肝下腔静脉血流，阐明肝脏再灌注损伤的限度及血液或脂质过氧化反应中前列腺素和内毒素的变化。将大鼠模型分为3组：缺血60分钟组（GroupI）、缺血120分钟组（GroupII）和肝灌注4^ C灵格液组（GroupII+肝灌注）。在肝动脉、门静脉及下腔静脉肝上、肝下段血流中断时，门静脉和下腔静脉淤滞血经送血泵分流至颈静脉。灌注时，向肝侧门静脉主静脉插入缺血肝闪管，经股静脉将肝脏灌注的液体引流至肝下腔静脉。1. 再灌注后5 d生存率分别为：I组83%，pii组14%，piii组43%，肝衰竭是所有非幸存者的主要死亡原因。2。 各组肝脏功能在再灌注后立即受损，幸存者在再灌注后3天恢复正常，非幸存者则加重。与I组和diii组相比，grupii组肝功能异常最为明显。3. 血中前列腺素：6-酮-前列腺素- f_ < 1α - > (6KF)在再灌注后立即升高，以pii组最高。第1组和第2组存活小鼠3h后6KF明显降低。另一方面，存活组血栓素B_2（TxB_2）较高，非存活组血栓素B_2在再灌注3h后迅速下降。因此，pii组在再灌注后立即出现TxB_2/6-KF低值，预后较差。4. 各组再灌注后血内毒素升高，3h后达到峰值，再灌注后逐渐降低；pii组的恢复明显延迟。5. 再灌注后血脂过氧化值偏高，但存活3天后血脂过氧化值恢复正常，与肝脏过氧化脂浓度相关。6. 肝组织血流在再灌注后2小时减少，在幸存者中恢复。在肝窦中，即使在第7天也观察到库普弗细胞肥大，但在第14天有所改善。这些发现为肝脏缺血的局限性和可逆性提供了有用的信息。少

The purpose of this study is to clarify the limit of reperfusion inJuries in the liver and the changes of prostanoid and endotoxin in the blood or lipid peroxidative reaction by interrupting not only hepatic blood inflow but also that in the hepatic inferior vena cava, using adult mongrel dogs. The experimental models were classified into 3 groups:GroupI (60-minute ischemia), GroupII (120-minute ischemia) and GroupIII (GroupII+liver perfusion with 4^ﾟC Ringer's solution). During interruption of blood flow in the hepatic artery, portal vein, and both superior and inferior hepatic portionof inferior vena cava, stasis blood in the portal vein and inferior vena cava were bypassed into the jugular vein using a blood delivery pump。 For perfusion, a catheter for ischemic liver flashing was inserted into the main portal vein toward the liver side and a catheter for drainage of fluid perfused from liver into the hepatic inferior vena cava via the femoral vein. 1. The survival rate of 5 days aft … More er reperfusion was 83% in Group I, 14% in GroupII, and 43% in GroupIII, and liver failure was the main cause of death in all non-survivors. 2。 Liver function was impared immediately after reperfusion in each group and normalized at 3days after reperfusion in the survivors but aggravated in the non-survivors. GorupII showed the most marked abnormality in liver function, comparing with Groups I andIII. 3. Prostanoid in blood : 6-keto-prostaglandin-F_<1alpha> (6KF) increased immediatelyafter reperfusion, and it showed highest value in GroupII. 6KF was decreased markedly after 3hours in the survivors of GroupI and II. On the other hand, thromboxane B_2(TxB_2 was high in the survivors but rapidly decresed 3hours after reperfusion in the non-survivors. Therefore TxB_2/6-KF was marked low value immediately after reperfusion in GroupII shown poorest prognosis. 4. Blood endotoxin increased after reperfusion in each group, reaching a peak after 3hours, but decreased thereafter ; the recovery in GroupII was significantly delayed. 5. Blood lipid peroxide was high after reperfunsion but was normalized after 3days in the survivors, being correlated with the lipid peroxide concertration in the liver. 6. Blood flow in the liver tissue decreased 2hours after reperfusion and recovered in the survivors. In sinusoids of the liver, Kupffer cell hyertrophy was observed even after 7days but improved by after 14days.These findings provide useful information on the limit and reversibility of ischemia in the liver. Less