Alabovskiĭ V V, Vinokurov A A, Dmitrashchuk A I
Vopr Med Khim. 1997 Jul-Aug;43(4):239-46.
The aim of investigation was to study the effects of extracellular sodium concentration on cardiomyocyte swelling and evaluation of this process in myocardial damage due to the calcium paradox. The experiments on isolated rat hearts showed that reperfusion by Ca- containing solution (Ca2+ 2.0 mM) after 10 minutes perfusion with Ca- free medium caused ameliration of water contents, depletion of high-energy phosphates, loss of myoglobin and uncoupling of respiration and phosphorylation in mitochondria. Either decreasing of sodium concentration (till 30-80 mM) or addition of strophant-hine (50 microM) resulted in exacerbation of calcium paradox (further augmentation of tissue water contents and increasing of cellular damage). Sucrose (240-340 mM), added low-sodium Ca- free solution was failed to prevent accumulation of water, loss of myoglobin and high- energy phosphates caused by subsequent perfusion with Ca- containing medium. Elevation of extracellular concentration of sodium ions (from 140 mM till 200-220 mM), but did not tonicity reduced cellular swelling, water accumulation in tissue, prevented loss of myoglobin and ATP, phosphocreatine level. The protective effect of hypersodium medium remained unchanged even sucrose was added to reperfusion solution to maintain osmotic pressure throuthout experiment. There are close correlation between intensity of water accumulation and degree of myocaridal damage during the calcium paradox, that confirms participant of Na- dependent cellular swelling in the development of cellular abnormalities due to calcium paradox.
本研究的目的是探讨细胞外钠浓度对心肌细胞肿胀的影响，并评估钙反常所致心肌损伤过程中的这一现象。对离体大鼠心脏进行的实验表明，在无钙培养基中灌注10分钟后，用含钙溶液（Ca2+ 2.0 mM）再灌注会导致含水量改善、高能磷酸盐耗竭、肌红蛋白丢失以及线粒体呼吸与磷酸化解偶联。降低钠浓度（至30 - 80 mM）或添加毒毛花苷（50 microM）都会导致钙反常加剧（组织含水量进一步增加以及细胞损伤加重）。在低钠无钙溶液中添加蔗糖（240 - 340 mM）并不能防止后续用含钙培养基灌注所导致的水分蓄积、肌红蛋白丢失和高能磷酸盐耗竭。细胞外钠离子浓度升高（从140 mM至200 - 220 mM），但不改变张力，可减轻细胞肿胀、组织中的水分蓄积，防止肌红蛋白和ATP、磷酸肌酸水平的丢失。即使在再灌注溶液中添加蔗糖以在整个实验过程中维持渗透压，高钠培养基的保护作用仍保持不变。在钙反常过程中，水分蓄积强度与心肌损伤程度之间存在密切相关性，这证实了钠依赖性细胞肿胀参与了钙反常所致细胞异常的发生发展。
