Sodium exchange was studied in the arterially perfused papillary muscle of the dog. Three kinetically defined phases accounted for all the myocardial sodium: phase 0 (vascular)-λo (exchange constant) = 3.6 min-1 phase 1 (interstitial)-λ1 = 0.62 min-1; phase 2 (intracellular)-λ2 < 0.020 min-1 in quiescent muscles. The phase 2 exchange rate was proportional to frequency of contraction and increased by approximately 0.004 min-1 for each 1 beat/min increment in rate in muscles demonstrating stable function. A sudden increase in frequency of contraction was followed by a marked increase in phase 2 sodium exchange if muscle function did not deteriorate. This increased exchange required 14 min to achieve a steady state. During this time active tension increased (positive staircase) and then declined to become stable as the sodium exchange stabilized. In muscles in which increased frequency of contraction produced a progressive decrease in active tension and contracture, sodium exchange failed to increase. The characteristics of sodium exchange are compared to those previously defined for calcium and potassium in the perfused dog papillary muscle. It is proposed that alteration in sodium exchange is a primary determinant of calcium and potassium movements and thereby plays a significant role in the control of myocardial contractility.

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