Drewnowska K, Clemo H F, Baumgarten C M
Department of Physiology, Medical College of Virginia, Richmond 23298-0551.
J Mol Cell Cardiol. 1991 Nov;23(11):1215-21. doi: 10.1016/0022-2828(91)90079-2.
During cardiac surgery, the heart is infused with cold crystalloid cardioplegic solutions such as St. Thomas' Hospital (StT) solution, which contains high concentrations of K+ and Mg2+. The high K+ and Mg2+ block impulse conduction and inhibit Ca2+ influx, thereby arresting the heart and reducing cardiac oxygen consumption. Nevertheless, myocardial edema and post-operative abnormalities have been noted after cardioplegia and attributed to ischemia and reflow or to hypothermia. We found, however, that cold StT (9 degrees C) was hypotonic and induced cell swelling in the absence of ischemic injury. Cell swelling in cold StT was not due to hypothermia alone, but rather was caused by KCl influx and was prevented by partially replacing Cl- with an impermeant anion. After exposure to cold StT, cells transiently shrank to less than control volume on rewarming in physiological saline (Tyrode's solution, 37 degrees C). The transient shrinkage was blocked by ouabain suggesting that Na+ loading of depolarized hypothermic cells and Na(+)-K+ pump activation on rewarming were responsible. Hypothermic ventricular cells seem to follow Donnan equilibrium, and the product of [K+] x [Cl-] in cardioplegic solutions affects cell volume in the absence of ischemic injury.
在心脏手术期间，心脏会被注入冷晶体心脏停搏液，如圣托马斯医院（StT）溶液，其含有高浓度的K⁺和Mg²⁺。高浓度的K⁺和Mg²⁺会阻断冲动传导并抑制Ca²⁺内流，从而使心脏停搏并减少心肌耗氧量。然而，心脏停搏后已观察到心肌水肿和术后异常情况，并归因于缺血再灌注或低温。然而，我们发现冷的StT（9℃）是低渗的，并且在没有缺血损伤的情况下会诱导细胞肿胀。冷StT中的细胞肿胀并非仅由低温引起，而是由KCl内流导致的，并且通过用非渗透性阴离子部分替代Cl⁻可以防止这种情况。暴露于冷StT后，细胞在生理盐水中（37℃的台氏液）复温时会短暂收缩至小于对照体积。哇巴因可阻断这种短暂收缩，这表明去极化低温细胞的Na⁺负载以及复温时Na⁺-K⁺泵的激活是造成这种情况的原因。低温心室细胞似乎遵循唐南平衡，并且心脏停搏液中[K⁺]×[Cl⁻]的乘积在没有缺血损伤的情况下会影响细胞体积。
