Strubelt O, Younes M
Institut für Toxikologie Medizinische Universität zu Lübeck, FRG.
Res Commun Chem Pathol Pharmacol. 1988 Sep;61(3):327-34.
Isolated perfused livers from fasted rats were subjected to 30 min of hypoxia followed by 60 min of reoxygenation. At a calcium concentration of 1.25 mmol/l in the perfusate, hypoxia induced injury as evidenced by a marked release of GPT and SDH into the perfusate and by an accumulation of calcium in the livers. Omission of calcium from the perfusate attenuated hypoxia-induced enzyme release by about 50% and prevented the increase of hepatic calcium completely. A complete protection of the liver against hypoxic injury was attained in the absence of calcium when Na2 EDTA was added. An influx of calcium from the extracellular to the intracellular fluid seems to be involved in but is not the sole cause of hypoxia-induced hepatic injury.
将禁食大鼠的离体灌流肝脏进行30分钟缺氧处理，随后再进行60分钟复氧处理。当灌流液中钙浓度为1.25 mmol/L时，缺氧诱导损伤，表现为谷丙转氨酶（GPT）和琥珀酸脱氢酶（SDH）大量释放到灌流液中以及肝脏中钙的蓄积。灌流液中去除钙可使缺氧诱导的酶释放减少约50%，并完全阻止肝脏钙含量的增加。当加入乙二胺四乙酸二钠（Na2 EDTA）时，在无钙情况下肝脏可完全免受缺氧损伤。细胞外钙流入细胞内液似乎参与了缺氧诱导的肝损伤，但并非其唯一原因。
