Kinetic Studies of Calcium Distribution in Ventricular Muscle of the Dog
Five phases (0 to 4) were defined kinetically for calcium in the dog papillary muscle vascularly perfused for five to six hours with perfusate containing 5 mM/liter calcium. The mean rate constant, λ, (min-1), approximate calcium concentration (mM/liter muscle water) and suggested origin of each phase are respectively: (0) λ0 = 3.5, 0.4, vascular; (1) λ1 = 0.59, 1.8, interstitial; (2) λ2 = 0.116, 1.7, "specialized" calcium transport system (?sarcoplasmic reticulum); (3) λ3 = 0.021, 2.0, intracellular; (4) λ approx 0.004, <1.6, intracellular and/or connective tissue. Inotropism, occuring coincidentally with institution of perfusion by solution containing 25% normal sodium concentration, was marked by a mean 60% increase in peak isometric tension and a mean 87% increase in rate of tension development. These inotropic changes stabilized within 10 minutes despite maintenance of low sodium perfusion and regressed within 10 minutes upon return to normal sodium perfusion. There was a mean 0.5 mM/liter change in calcium concentration of the muscle associated with the inotropic changes. This fraction of tissue calcium could be ascribed entirely to kinetically-defined phase 2 and was freely exchangeable. Prolonged (40-minute) low sodium perfusion resulted in no inotropic changes beyond the first 10 minutes but was associated with a continued marked net increase in muscle calcium. This fraction of tissue calcium was irreversibly bound and inexchangeable. It was suggested that this fraction of calcium may be bound as its phosphate salt.
The possibility that the Ca++ content of the "specialized system" represented by phase 2 is controlled by movements of Na+ into and out of this system is discussed. Ca++ movements associated with increased frequency of contraction are also discussed in the context of their possible relation to Na+ exchange.
- Received April 27, 1964.
- © 1964 American Heart Association, Inc.