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- W603191726 abstract "SEVERAL investigators have reported that calcium channel blockers may protect the liver from anoxic injury or from other hepatotoxic agents.1,2 Because the putative protective effects of calcium channel blockers have been obtained in perfused whole liver, it is impossible to determine which cells within the liver were actually the target of the calcium antagonists: vascular smooth muscle cells, endothelial cells, Kupffer cells, or parenchymal cells. In addition, most of the protective effects observed have occurred after reoxygenation and not during anoxia, suggesting that calcium antagonists act to prevent reperfusion injury and not anoxic injury. The objective of the present experiments was to determine whether calcium channels are involved in the damage induced by anoxia in perfused isolated rat hepatocytes. Specifically the studies described were designed to determine whether the massive rise in cytosolic-free calcium (Cai2+) and the increase in loss of cytosolic lactate dehydrogenase (LDH) evoked by anoxia can be blocked by specific Ca2+ channel blockers. Three classes of Ca2+ antagonists (nifedipine, verapamil, and diltiazem) were studied. Each was studied at his Ki (10−7) and at concentrations 10 and 100 times above Ki." @default.
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- W603191726 date "1992-12-01" @default.
- W603191726 modified "2023-09-23" @default.
- W603191726 title "Anoxia/reoxygenation injury in hepatocytes is not prevented by calcium channel blockers." @default.
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