Contraction and relaxation of isolated cardiac myocytes of the frog under varying mechanical loads.
The mechanics of cardiac systole and relaxation have been studied primarily at the level of the whole heart or intact muscle. End-systolic pressure-volume relations of frog hearts have been found to be load dependent, whereas those of the mammal are relatively load independent. On the other hand, myocardial relaxation as studied at the muscle level is load independent in the frog but markedly load dependent in the mammal. Interpretation of these studies is complicated because of the unknown contribution of extracellular connective tissue, neurohumoral factors, and, in the case of the heart, the complex chamber geometry. Therefore, it is valuable to study cardiac mechanics at the level of the basic unit of contractile activity--the isolated myocyte. The goal of this study was to subject isolated frog cardiomyocytes to mechanical loading paradigms that mimic those presented to the cells within the heart. In the first part of this study, the afterload and preload of contracting cells were varied to study their effects on the end-systolic force-length relation, which was consistently found to be load independent over the range of isotonic shortening tested (typically 5%). We also investigated the force-length-time response of the cells to test the concept of the heart behaving as a time-varying elastance. Our results suggest that in this regard the frog myocyte behaves like mammalian muscle, and they are consistent with the presence of a small viscosity within the cell. We conclude that the tissue structure of the frog heart may contribute to disparity in mechanical behavior at the different structural levels. In the second part of this study, we subjected isolated frog cardiomyocytes to four different loading paradigms to test the hypothesis that myocardial relaxation in the frog is independent of load. These sequences consisted of afterloaded contractions followed by conventional isotonic-isometric relaxation (ACCR) or afterloaded contractions followed by physiologically reversed isometric-isotonic relaxation (ACPR). Relaxation was measured under isometric conditions using a variable afterload with either the ACCR or ACPR paradigms. The decay of force was independent of the cell length at which it occurred or the amount of shortening prior to it within the contractile cycle. Relaxation also was measured as relengthening of the cell under isotonic late-load conditions, using the ACPR paradigm either with a variable afterload or variable late load. Relengthening had a time course that was unaffected by changes in afterload (i.e., extents of shortening) or late load (equivalent to the filling pressure for the heart).(ABSTRACT TRUNCATED AT 400 WORDS)
- Copyright © 1993 by American Heart Association