Myocardial K⁺ repletion and rise in contractility after brief ischemic periods in the pig

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.