Ricci R L, Crawford S S, Miner P B
Gastroenterology. 1981 Jun;80(6):1445-50.
We studied the acute an chronic effects of ethanol on hepatic Na+, K+-ATPase activity. Graded doses of ethanol given 1 h before death acutely increased Na+, K+-ATPase activity in a dose-related manner to a maximum of 138% of control with a simultaneous serum ethanol of 35.4 mM (163 mg%). Rats chronically fed 10% ethanol as their only fluid for 5 days had normal Na+, K+-ATPase activity, however, when ethanol was withdrawn 14 h before death Na+, K+-ATPase activity fell to 60% of control. The in vitro addition of ethanol to membrane preparations from untreated rats caused an increase in Na+, K+-ATPase activity with ethanol concentrations less than 81 mM with decreased activity at higher concentrations. In membranes from rats treated chronically with ethanol Na+, K+-ATPase activity did not respond to in vitro ethanol while the decreased activity noted after ethanol withdrawal was reversed by in vitro ethanol. These results suggest hepatocytes respond to the acute effects of ethanol by membrane adaptation which restores Na+, K+-ATPase activity to normal in the presence of ethanol. This adaptive response is probably due to changes in membrane lipids modulating membrane fluidity.
我们研究了乙醇对肝脏钠钾ATP酶活性的急性和慢性影响。在死亡前1小时给予不同剂量的乙醇，可使钠钾ATP酶活性呈剂量依赖性急性增加，最高可达对照组的138%，同时血清乙醇浓度为35.4 mM（163 mg%）。以10%乙醇作为唯一液体长期喂养大鼠5天，其钠钾ATP酶活性正常，然而，在死亡前14小时停止给予乙醇后，钠钾ATP酶活性降至对照组的60%。在体外，向未处理大鼠的膜制剂中添加乙醇，当乙醇浓度低于81 mM时，钠钾ATP酶活性增加，而在较高浓度时活性降低。在长期用乙醇处理的大鼠的膜中，钠钾ATP酶活性对体外乙醇无反应，而在停止给予乙醇后观察到的活性降低可被体外乙醇逆转。这些结果表明，肝细胞通过膜适应对乙醇的急性作用作出反应，在有乙醇存在的情况下将钠钾ATP酶活性恢复到正常水平。这种适应性反应可能是由于膜脂质的变化调节了膜流动性。
