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Calcium exchange was studied in the arterially-perfused papillary muscle of the dog under the conditions of varying frequency of contraction as well as calcium-free perfusion. The following conclusions are drawn from these studies: (1) The maximum increment in rate of Ca++ uptake associated with increased rate of contraction occurs in the first 10 to 12 minutes following rate increase. The mean increment over this period of time is 2.5 μmoles/liter tissue water/beat. (2) The increased Ca++ exchange which occurs in association with the increases in rate of contraction occurs within that portion of the myocardium represented kinetically by phase 2. (3) The Ca++ associated with phase 2 remains reversibly bound. The maximum capacity of the “phase 2 system” under the present experimental conditions, is approximately 3.2 mmoles Ca++/liter tissue water. (4) Exceeding the capacity of the “phase 2 system” for Ca++ is associated with the onset of contracture in the muscle. This occurs at rates of contraction which produce progressive fall in contractile tension and is associated, presumably, with myocardial hypoxia. That fraction of Ca++ taken up in excess of the capacity of the “phase 2 system” is released very slowly. (5) The initial increment of Ca++ uptake, following an increase in rate, is reversed if the rate increment is not associated with progressive fall in systolic tension and contracture. (6) The maintenance of the ability to develop contractile tension depends significantly upon the presence of Ca++ in the “phase 2 system.”. The rate of loss of contractile tension is very nearly the same as the rate of loss of Ca++ from this system. (7) Ca++ exchange between vascular and interstitial regions depends upon concentration gradient. In contrast, Ca++ exchange of phases 2 and 3 (? sarcotubular system and intracellular region respectively) is unaffected by change of concentration gradient.

Calcium Exchange in Dog Ventricular Muscle: Relation to Frequency of Contraction and Maintenance of Contractility