Experimental Myocardial Ischemia Dynamic Alterations in Ventricular Contractility and Relaxation with Dissociation of Speed and Force in the Isovolumic Dog Heart

Although the time course of changes in myocardial function during ischemia has been demonstrated for tbe papillary muscle, this time course in tbe intact heart is less well understood. Accordingly, in 24 isolated, isovolumic, perfused dog hearts, coronary perfusion pressure (PP) was lowered to various fixed levels. Left ventricular developed pressure (LVP) rapidly fell and reached 63 ± 3% of control at 1 minute of ischemia and 50 ± 5% at 6 minutes; this was due primarily to an abbreviation of time to peak tension (TPP). dP/dt was 70 ± 3% of control at 1 minute and 56 ± 5% at 6 minutes. The rate of relaxation as reflected by negative dP/dt declined as well to 49 ± 4% of control at 1 minute of ischemia and to 41 ± 4% of control at 6 minutes. These changes were directly correlated with the decrease in PP. When PP was restored to normal, an overshoot of LVP and dP/dt was noted, peaking at 1 minute, returning to control by 5 minutes, and then gradually declining to 90 ± 2% of control following 25 minutes of recovery. Depression of the rate of relaxation was reduced, but persisted throughout recovery. Diminution of force development early in ishcemia is due primarily to decreased duration of contraction accompanied by a decrease in relaxation rate. Later, the rate of force development also falls, but some preservation of force development may result from the return toward normal of tbe duration of contraction.