Anoxia/reoxygenation injury in hepatocytes is not prevented by calcium channel blockers.
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چکیده
منابع مشابه
Major Differences in Ca$‘+ Response to Anoxia between Neonatal and Adult Rat CA1 Neurons: Role of Ca:+ and Nag
Although we and others have previously shown that newborn central mammalian neurons are more tolerant to anoxia than their adult counterparts, we do not know whether neonatal nerve cells accumulate free cytosolic calcium (Cat+) less than adults in response to 0, deprivation. In order to determine whether anoxia increases Ca:+ in adult and neonatal neurons, we monitored calcium in CA1 hippocampa...
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AN increase in the concentration of the intracellular calcium ion within hepatocytes has been proposed by several investigators as the explanation for the pathologic events that occur during anoxic and reperfusion injury. Nonnally the concentration of cytosolic-free calcium (Ca/+) is maintained at a physiologic low level by energy-dependent transport systems. Anoxic conditions, which are known ...
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The occurrence of biliary stricutures in allografts following liver transplantation correlates with the duration of preservation time. The correlation between preservation time and biliary strictures suggests that anoxic or reperfusion injury of the bile duct epithelium causes stricture formation. However, the relative susceptibility of bile duct cells to anoxic or reoxygenation injury is unkno...
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متن کاملMitochondrial permeability transition in rat hepatocytes after anoxia/reoxygenation: role of Ca2+-dependent mitochondrial formation of reactive oxygen species.
Onset of the mitochondrial permeability transition (MPT) is the penultimate event leading to lethal cellular ischemia-reperfusion injury, but the mechanisms precipitating the MPT after reperfusion remain unclear. Here, we investigated the role of mitochondrial free Ca(2+) and reactive oxygen species (ROS) in pH- and MPT-dependent reperfusion injury to hepatocytes. Cultured rat hepatocytes were ...
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ورودعنوان ژورنال:
- Transplantation proceedings
دوره 24 6 شماره
صفحات -
تاریخ انتشار 1992