ABSTRACT
The aim of the present investigation was to examine the conditions inducing a calcium paradox in the isolated perfused pigeon heart. Loss of mechanical and electrical activity, creatine phosphokinase and total protein release were used to define cell damage. Perfusion was performed at 36, 38, 40 and 42 degrees C and calcium deprivation lasted 5, 10, 20 or 40 min. At low temperatures even prolonged calcium depletion failed to induce a calcium paradox. After a 40 min calcium depletion at normal body temperature (42 degrees C) ventricular activity ceased and a major contraction occurred followed by an increase in resting tension. During the 20-min reperfusion period the release of creatine phosphokinase was 267.18 +/- 0.8 IU/g of dry wt and the total amount of protein loss was 109.3 +/- 1.0 mg/g of dry wt, while lower temperatures resulted in a decreased loss of protein and creatine phosphokinase. Using two different Tyrode's perfusion buffers instead of normal bicarbonate ones, a protection of the pigeon heart against the induction of this phenomenon was observed. Furthermore, acidosis as well as alkalosis protected the heart as estimated by the significant recovery of electromechanical activity, and the quite low total protein and creatine phosphokinase losses. The results of this study suggest that the basic mechanisms and damaging effects of calcium overloading are common in mammalian and pigeon hearts.
