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Underlying mechanisms of afterload dependency of ventricular relaxation rate were studied in nine isolated canine hearts and nine open chest dogs. In isolated hearts with isobaric contraction, peak LV pressure was increased by volume loading with stroke volume unchanged, and in anesthetized open chest dogs the afterload was altered by a manual clamp of the descending aorta to various extent under the pharmacological blockade of the autonomic nerve activity. Ventricular relaxation rate was assessed by the time constant (T) of isovolumic LV pressure decay. In hearts in situ of open chest dogs, T was progressively (p less than 0.01) increased as peak LV pressure increased, whereas in isolated hearts T was decreased as afterload increased (p less than 0.05), indicating that peak LV pressure is not a major determinant of ventricular relaxation rate. Between these two heart preparations loading sequence of the heart during contraction was characteristically different; in open chest dogs, as afterload increased ejection timing was accelerated and the time of peak LV pressure (TPmax) was prolonged, whereas TPmax in isolated hearts was decreased and ejection timing was progressively delayed as an increase in afterload. Consequently, TPmax showed a high correlation with T irrespective of peak LV pressure. These results indicate that T is directly dependent on loading sequence mainly regulated by ejection timing. This finding was also confirmed in open chest dog experiments in which 20 pairs of contractions with comparable peak LV pressures and LV dimensions (end-systolic and end-diastolic lengths) but characteristically different loading conditions during contraction (early maximal loading vs late maximal loading) were obtained by the manual clamp of ascending aorta; in early maximal loading conditions (TPmax: 185 +/- 8 ms) T's (66 +/- 3 ms) were significantly (p less than 0.01) smaller than those (110 +/- 10 ms) in late maximal loading conditions (TPmax: 261 +/- 11 ms). A change in loading sequence associated with afterload interventions in hearts in situ may be due to a change in compliance in peripheral arterial system. We conclude that afterload dependency of ventricular relaxation rate observed in hearts in situ could be attributed to the accompanied changes in loading sequence of the heart probably due to a change in arterial compliance. The dependency of relaxation on loading sequence of the heart might be clinically important in evaluating the effect of cardiovascular agents on ventricular relaxation since these agents may largely affect the vascular compliance as well as muscular relaxation per se.

Altered loading sequence as an underlying mechanism of afterload dependency of ventricular relaxation in hearts in situ.