| Autor: |
Alabovskiĭ VV; Voronez State Medical Academy, 394022, Voronez, Studencheskaya St., 10. Russia., Khamburov VV, Vinokurov AA |
| Jazyk: |
ruština |
| Zdroj: |
Rossiiskii fiziologicheskii zhurnal imeni I.M. Sechenova [Ross Fiziol Zh Im I M Sechenova] 2003 Dec; Vol. 89 (12), pp. 1538-50. |
| Abstrakt: |
It is well-known that the first stage of the calcium paradox involves decreasing of Na+ gradient. The decreased sodium gradient is a cause of activation of the Na(+)-Ca+ exchange and formation of cardiac injury during the calcium repletion. Potassium ions are natural extracellular activators of Na(+)-pump. It has been shown that heart perfusion by Ca(2+)-free medium evoked extrusion from cells of hydrophilic amino acids whose transport-depends on sodium gradient. The heart reperdusion with Ca(2+)-containing agent leads to myofibrillar contracture and extensive myoglobin release. The simultaneous events are: elevation in tissue water contents, decreasing of intracellular concentration of adeninnucleotides, uncoupling of oxidation and phosphorylation in mitochondria. The decreasing of K+ level to 0.5 mM exacerbates myocardial damage during the calcium paradox, despite absence of myocardial contracture. The elevation of K+ (to 10 mM or 20 mM) attenuated the calcium paradox development in the heart. The elevated K+ concentration protected isolated heart from extensive myoglobin release, development of myocardial contracture. The high K+ concentrations alleviate mitochondrial damage and elevate contents of adeninnucleotide in the tissue. The positive effect of the elevated K+ concentration can be completely blocked by strophanthine, the selective Na+, K(+)-pumb blocker. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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