Potassium in Dog Ventricular Muscle: Kinetic Studies of Distribution and Effects of Varying Frequency of Contraction and Potassium Concentration of Perfusate
Four phases (0 to 3) were defined kinetically for potassium in the dog papillary muscle when perfused arterially for four to five hours with solution containing 4 mM/liter K+. Total tissue K+ fell from 91.1±1.99 to 41.0±1.06 mmoles/liter after three hours perfusion. It then remained stable during the period when kinetic studies were done. The mean rate constant λ (min-1), potassium content (mmoles/liter tissue water) and suggested origin of each phase are respectively: (phase 0) λ0 = 3.2, 0.3, vascular; (phase 1) λ1 = 0.65, 2.06, interstitial; (phase 2) λ2 = 0.0139, 39.3, intracellular; (phase 3) λ3 < 0.004, <0.5, origin unknown.
Alteration of K+ concentration in perfusing fluid produced significant changes in the intracellular exchange rate of K+. This was in marked contrast to increments in frequency of contraction which had no effect on the overall exchangeability of intracellular potassium. Increases in rate, however, were associated with a transient net loss of intracellular K+. This loss continued if the active tension of the muscle declined and if contracture progressed. The loss ceased if muscle function remained stable during continued increased frequency of contraction. A positive tension staircase was approximately proportional to the net K+ loss. The net K+ loss was 0.93 mmole/liter tissue water in nine muscles in which a mean 27 beats/min rate increment was introduced for a mean of 16 minutes. This represented 2.4% of intracellular K+.
A significant time lag was found before the net K+ loss reached a maximum rate and began to decline. This is compared with the previously demonstrated transient net increment in Ca++ uptake that accompanies increased frequency of contraction. These ionic movements are consistent with the theory that Na+ movements in and out of a "specialized membrane region" are related to Ca++ movements and thereby influence the control of myocardial contractility.
- Accepted August 2, 1965.
- © 1966 American Heart Association, Inc.