Ishikawa N
First Department of Surgery, Nippon Medical School, Tokyo, Japan.
Nihon Geka Gakkai Zasshi. 1993 Mar;94(3):242-9.
The present study was designed to indicate the role of ET-activated PMN on hepatocyte injury during ET shock. In this study ET shock was made by intravenous administration of 5mg/kg ET to rats. PMN and plasma were sequentially collected from rats before and 6, 12, 24 hours after administration of ET. Hepatocytes were collected from rats without administration of ET. Plasma glutamate dehydrogenase, peripheral PMN counts and superoxide production of PMN were higher at 12 hours than the value of before and at 6, 24 hours. Cell damages and the infiltration of PMN into the liver were most remarkable at 12 hours. Phagocytosis of PMN was lower only at 6 hours than the value of before. In vitro, the hepatocyte cytotoxicity of PMN reached a peak at 12 hours, but was not found at 24 hours. The findings suggested that the microcirculatory insufficiency and ET-activated PMN played important roles of hepatocyte injury during ET shock.
本研究旨在阐明内毒素（ET）激活的中性粒细胞（PMN）在ET休克期间对肝细胞损伤的作用。在本研究中，通过给大鼠静脉注射5mg/kg ET制造ET休克。在注射ET之前以及注射后6、12、24小时依次采集大鼠的PMN和血浆。从不注射ET的大鼠采集肝细胞。血浆谷氨酸脱氢酶、外周PMN计数以及PMN的超氧化物生成在12小时时高于注射前以及6、24小时时的值。细胞损伤以及PMN向肝脏的浸润在12小时时最为显著。PMN的吞噬作用仅在6小时时低于注射前的值。在体外，PMN的肝细胞细胞毒性在12小时时达到峰值，但在24小时时未发现。这些发现提示，微循环功能不全和ET激活的PMN在ET休克期间对肝细胞损伤起重要作用。
