VOPROSY MEDITSINSKOI KHIMII (ISSN 0042-8809)

Effect of extracellular sodium concentration on cardiomyocyte swelling and myocardial damage during the calcium paradox

   
Alabovsky V.V., Vinokurov A.A., Dmitrachshuk A.I.
PubMed Id: 9312939
Year: 1997  Volume: 43  Issue: 4  Pages: 239-246
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 жM) 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- enegry 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 myocardial damage during the calcium paradox, that confirms participance of Na- dependent cellular swelling in the development of cellular abnormalaties due to calcium pafadox.
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Keywords: heart, calcium, energy metabolism, calcium paradox
Citation:

Alabovsky, V. V., Vinokurov, A. A., Dmitrachshuk, A. I. (1997). Effect of extracellular sodium concentration on cardiomyocyte swelling and myocardial damage during the calcium paradox. Voprosy Meditsinskoi Khimii, 43(4), 239-246.
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