Potassium loss from the myocardium during brief ischemic periods is well documented, but whether intrinsic myocardial mechanisms restore this loss during reperfusion is unclear. To address this question, we established a shunt from the coronary sinus to the right atrium in seven open-chest pigs. Shunt flow and arterial and coronary sinus potassium concentrations were measured continuously in order to determine myocardial potassium balance. Thirty, 60 and 120 s occlusions of the mid-LAD coronary artery were repeated four times each at 10 min intervals with reproducible metabolic and hemodynamic responses. A myocardial K+ reuptake amounting to 51 to 77% of K+ release during ischemia occurred between 20 and 140 s of reperfusion. The maximal rate of K+ reuptake was 1.4 (0.7 to 3.6), (median and 95% confidence interval), 4.3 (2.5 to 9.6) and 7.3 (4.9 to 13.4) μmol/100 g min after occlusion periods of 30, 60 and 120 s, respectively. Concomitant with the K+ reuptake a progressive rise in LV dP dt occurred. Adrenoceptor stimulation could not explain these findings since catecholamine release declined during occlusion and reperfusion. We suggest that increased intracellular Na+ concentration in early reperfusion stimulates the Na,K-pump and favours Ca++ entry through Na+ Ca++ exchange, thereby mediating K+ reuptake and the rise in contractility.
- Contractility: In vivo
- Ionic balance
ASJC Scopus subject areas
- Molecular Biology
- Cardiology and Cardiovascular Medicine