ISCHEMIC-INJURY IN LIVER-TRANSPLANTATION - DIFFERENCE IN INJURY SITES BETWEEN WARM AND COLD ISCHEMIA IN RATS
ISCHEMIC-INJURY IN LIVER-TRANSPLANTATION - DIFFERENCE IN INJURY SITES BETWEEN WARM AND COLD ISCHEMIA IN RATS
复制标题
DOI：
10.1002/hep.1840160226
复制
发表时间：
1992-08-01
期刊：
影响因子：
13.5
通讯作者：
SUGIMACHI, K
中科院分区：
文献类型：
--
作者：
IKEDA, T;YANAGA, K;SUGIMACHI, K
使用热缺血或冷缺血的同种异体肝移植物，我们评估了大鼠移植模型中肝细胞、肝窦内皮细胞和库普弗细胞的功能和形态变化。所有接受 4 小时冷缺血或 30 分钟热缺血的同种异体移植物的接受者均存活超过 22 天，并被判断为存活。另一方面，所有接受6小时冷缺血或60分钟热缺血的移植物受体均在2天内死亡，因此被判断为无法存活。利用这些存活和非存活的同种异体移植模型，通过胆汁排出量和血清谷氨酸草酰乙酸转氨酶、血清谷氨酸丙酮酸转氨酶和血清乳酸脱氢酶水平评估肝细胞功能；通过血清透明质酸水平判断内皮细胞功能，通过静脉胶体碳清除试验测定库普弗细胞功能。肝细胞损伤是热缺血移植物的显着特征，尤其是非存活移植物。另一方面，与有活力的对应组相比，无活力的冷缺血组的血清透明质酸值显着较高，这表明内皮细胞的功能抑制在冷的、无活力的肝脏中占主导地位。组织学检查与上述结果一致。热缺血或冷缺血组的库普弗细胞的吞噬活性均降低，而热缺血组库普弗细胞的数量减少。我们得出的结论是，在同种异体肝移植中，热缺血时的主要损伤部位是肝细胞，并表明冷缺血与内皮细胞损伤有关。
Using liver allografts with warm or cold ischemia, we evaluated functional and morphological alterations in hepatocytes, sinusoidal endothelial cells and Kupffer cells in a rat transplantation model. All recipients of allografts with either 4 hr of cold or 30 min of warm ischemia lived more than 22 days and were judged viable. On the other hand, all recipients of grafts with 6 hr of cold or 60 min of warm ischemia died within 2 days and were therefore judged to be nonviable. With these viable and nonviable allograft models, hepatocyte function was evaluated by the bile output and serum glutamic-oxaloacetic transaminase, serum glutamic-pyruvic transaminase and serum lactate dehydrogenase levels; endothelial cell function was judged by the serum hyaluronic acid level, and Kupffer cell function was measured by an intravenous colloidal carbon clearance test.Hepatocyte injury was the prominent feature in warm ischemic grafts, especially in the nonviable ones. On the other hand, serum hyaluronic acid values were significantly higher in the nonviable cold ischemic group, compared with the viable counterpart, suggesting that the functional depression of endothelial cells was predominant in cold, nonviable livers. Histological examinations coincided with the above findings. The phagocytic activity of Kupffer cells was depressed by warm or cold ischemia, whereas the number of Kupffer cells was reduced in the warm ischemia group. We conclude that in liver allografts the main site of injury in warm ischemia is the hepatocytes and suggest that cold ischemia is associated with endothelial cell damage.