Blachley J D, Johnson J H, Knochel J P
Am J Med Sci. 1985 Jan;289(1):22-6. doi: 10.1097/00000441-198501000-00004.
The deleterious effects of ethanol on a variety of tissues may result largely from altered ion permeabilities and transport. Clinically relevant ethanol concentrations in blood increase the sodium permeability of the plasma membrane and depress active sodium transport by suppressing Na, K-ATPase activity. As a result, intracellular sodium concentration increases. The total tissue content of calcium increases. Important transport mechanisms deranged by ethanol probably include those regulating calcium-sodium and hydrogen-sodium exchange at the plasma membrane and calcium uptake by the sarcoplasmic reticulum. A modest decline in magnesium content of muscle occurs after chronic exposure to ethanol. This also has been associated with accumulation of calcium. After days to weeks of sustained ethanol intake, sodium pump activity, active sodium transport and tissue oxygen consumption increase. The cell membrane potential, initially lowered by alcohol, increases to supraphysiological levels. This is likely an electrogenic effect of increased sodium transport in response to a sodium leak. Eventually the earlier derangements in tissue composition, including retention of sodium, chloride, and calcium, and reductions in magnesium, potassium, and phosphate, slowly undergo correction. This biphasic response of injury and adaptation appears to depend upon adequate nutrition and the absence of other factors that can adversely affect cell function. That the Na, K-ATPase activity and oxygen consumption remain elevated suggests an ongoing sodium leak of the sarcolemmal membrane. Chronic ethanol-induced cell necrosis may be related to the increased intracellular calcium that accompanies the increase in sodium permeability. Conceivably, critically elevated concentrations of calcium in the cytoplasm may activate autolytic enzymes that in turn may be responsible for structural damage to the cell.
乙醇对多种组织的有害影响可能主要源于离子通透性和转运的改变。临床上血液中与乙醇相关的浓度会增加质膜的钠通透性，并通过抑制钠钾 -ATP 酶活性来抑制主动钠转运。结果，细胞内钠浓度升高。组织中钙的总含量增加。乙醇扰乱的重要转运机制可能包括调节质膜上钙 - 钠和氢 - 钠交换以及肌浆网对钙摄取的机制。长期接触乙醇后，肌肉中的镁含量会适度下降。这也与钙的积累有关。持续摄入乙醇数天至数周后，钠泵活性、主动钠转运和组织氧消耗增加。最初因酒精而降低的细胞膜电位会升高到超生理水平。这可能是由于钠泄漏导致钠转运增加而产生的电生效应。最终，组织成分早期的紊乱，包括钠、氯和钙的潴留以及镁、钾和磷酸盐的减少，会慢慢得到纠正。这种损伤和适应的双相反应似乎取决于充足的营养以及不存在其他可能对细胞功能产生不利影响的因素。钠钾 -ATP 酶活性和氧消耗持续升高表明肌膜存在持续的钠泄漏。慢性乙醇诱导的细胞坏死可能与钠通透性增加伴随的细胞内钙增加有关。可以想象，细胞质中钙浓度的严重升高可能会激活自溶酶，进而可能导致细胞的结构损伤。
