Kurita K, Tanabe G, Aikou T, Shimazu H
First Department of Surgery, University of Kagoshima, School of Medicine, Japan.
J Hepatol. 1993 Jun;18(2):196-204. doi: 10.1016/s0168-8278(05)80246-6.
Regions of calcium accumulation were studied by 45Ca-autoradiography and microdensitometry during liver ischemia and reperfusion in rats. In autoradiographic studies 45Ca accumulated in all zones of the liver lobuli after 1-2 h of liver ischemia and 1, 3 and 6 h of reperfusion, but did not accumulate in non-ischemic liver lobes. Significant 45Ca accumulation occurred only with reperfusion after 1 or 2 h of liver ischemia. In the presence of reperfusion, 45Ca accumulation correlated with the length of ischemia. In histopathologic studies, liver necrosis was absent in lobuli after 1-h reperfusion. Some liver necrosis was observed in the group reperfused for 3 h and widespread liver necrosis appeared after 6-h reperfusion. Regions of 45Ca accumulation coincided with sites of microscopic liver cell damage and necrosis. These results suggested that calcium accumulation might be responsible for the liver cell damage induced by ischemia with reperfusion, that the intensity of calcium accumulation in 45Ca-autoradiograms indicates the degree of ischemia damage, and that the primary event leading to hepatocellular necrosis might be calcium accumulation and subsequent liver cell death.
在大鼠肝脏缺血和再灌注期间，通过45Ca - 放射自显影术和微量密度测定法研究了钙积累区域。在放射自显影研究中，肝脏缺血1 - 2小时以及再灌注1、3和6小时后，45Ca在肝小叶的所有区域积累，但在未缺血的肝叶中不积累。仅在肝脏缺血1或2小时后的再灌注时才出现显著的45Ca积累。在存在再灌注的情况下，45Ca积累与缺血时间相关。在组织病理学研究中，再灌注1小时后肝小叶中无肝坏死。在再灌注3小时的组中观察到一些肝坏死，而再灌注6小时后出现广泛的肝坏死。45Ca积累区域与微观肝细胞损伤和坏死部位一致。这些结果表明，钙积累可能是缺血再灌注诱导肝细胞损伤的原因，45Ca放射自显影图中钙积累的强度表明缺血损伤的程度，并且导致肝细胞坏死的主要事件可能是钙积累和随后的肝细胞死亡。
