Shibayama Y, Asaka S, Nishijima A
Department of Pathology, Osaka Medical College, Japan.
Exp Mol Pathol. 1991 Dec;55(3):251-60. doi: 10.1016/0014-4800(91)90005-i.
To clarify whether ischemic liver injury is due to ischemia itself or reperfusion, histopathological and functional changes in the liver were examined before and after liver ischemia in rats with porto-systemic collateral channels. Effects of oxygen-derived free radical scavengers or an inhibitor of platelet aggregation on development of ischemic liver injury were also examined. Liver ischemia was produced by ligation of the portal vein and hepatic artery at liver hilum for 1 hr. The primary lesion of ischemic liver injury was cloudy swelling of liver cells in the periportal and midzonal regions; it developed during ischemia. The cloudy swelling of liver cells induced uneven distribution of sinusoidal blood flow after reperfusion, and consequently individual liver cell necrosis and focal hepatocellular necrosis in the midzonal regions developed later. Elevation of cytoplasmic enzyme activities in the serum after reperfusion was due to leakage across the damaged plasma membrane of liver cells. The treatment with superoxide dismutase, catalase, or heparin had not altered the liver injury that was attributed to ischemia, biochemically and histologically. These results suggest that ischemic liver injury is due to liver cell damage developed during ischemia, and that the ischemic liver injury is not alleviated or prevented by superoxide dismutase, catalase, or heparin.
为了阐明缺血性肝损伤是由于缺血本身还是再灌注引起的，对具有门体侧支循环的大鼠肝缺血前后的肝脏组织病理学和功能变化进行了检查。还研究了氧衍生自由基清除剂或血小板聚集抑制剂对缺血性肝损伤发展的影响。通过在肝门处结扎门静脉和肝动脉1小时来造成肝脏缺血。缺血性肝损伤的主要病变是门静脉周围和中区区域肝细胞的浊肿；它在缺血期间发展。肝细胞的浊肿在再灌注后导致肝窦血流分布不均，随后中区区域出现单个肝细胞坏死和局灶性肝细胞坏死。再灌注后血清中细胞质酶活性升高是由于肝细胞受损的质膜渗漏所致。超氧化物歧化酶、过氧化氢酶或肝素治疗在生化和组织学上均未改变归因于缺血的肝损伤。这些结果表明，缺血性肝损伤是由于缺血期间发生的肝细胞损伤所致，并且超氧化物歧化酶、过氧化氢酶或肝素不能减轻或预防缺血性肝损伤。
