By perfusing the isolated turtle heart with Cs solution, most of the intracellular K can be replaced by Cs. After 3--4 hr, Cs approaches a steady-state distribution with a concentration slightly below initial K concentration. 2. During the initial stages of perfusion, the heart accumulated Cs and lost K, the exchange ratio of K for Cs was estimated to be about 0.6. Subsequently perfusion yielded an equi-ionic substitution of K by Cs. 3. In presence of DNP (2 x 10(-4) M), K efflux and Cs accumulation increased but the low initial K--Cs exchange was abolished. Then, the replacement of K by Cs took place at a ratio of K:Cs of about 0.8. Ouabain (10(-5) M) suppressed uptake of Cs whereas K loss was the same as with DNP. 4. These results confirm that permeability of the cardiac sarcolemma to Cs is low, and suggest that the movement of Cs must be mainly attributed to its active transport into cells by the ionic exchange which normally transports K+ and is coupled to the extrusion of Na. The initial low net K efflux could be explained by an accumulation process which facilitates retention of K by the heart. A mechanism of this kind would be described as active reabsorption of some K present in extracellular space and would consequently reduce the uptake of Cs. 5. After loading the heart with Cs, perfusion with K solution showed the exchange of Cs for K at a ratio of Cs:K of about 0.5. K reaccumulation is reduced by ouabain (10(-5) M) and comes back to a normal steady-state distribution after 5 hr. At this time, K concentration was slightly below normal K value, but only half Cs content was eliminated. After 15 hr of perfusion, intracellular K remained constant whereas 15% of the original Cs remained.
