Uncoupling of Muscle Shortening from Contractile Force in Intact Heart

It is well accepted that myocardial segment shortening is preceded by, and dependent upon, development of isometric force. In other words, muscle shortening is coupled in both time and amplitude to force; therefore it is assumed that dysfunctional contraction (e.g., in stunned myocardium) must be due to depressed contractility. However, it is also possible that dysfunctional shortening would result from poor coupling between force and shortening. This study was designed to test this hypothesis, and to show that it is possible to reversibly dissociate shortening from force development under certain conditions. In open-chest anesthetized dogs, 2,3-butanedione monoxime (BDM), acetylcholine and dobutamine were each injected directly into the left anterior descending coronary artery (LAD). The LAD was then ligated for 10 min to produce local myocardial ischemia, followed by reperfusion. In addition to global hemodynamics, regional myocardial force and segment shortening were measured in both the LAD-perfused area and that perfused by the circumflex coronary artery which served as a control area. It was found that both BDM and postischemic reperfusion produced significantly reduced fiber shortening (from 17.1± 1.5% to 5.4± 1.1% and 6.5± 2.3% respectively), but regional force was not depressed (from 11.1± 1.3 to 22.5± 2.6 g and 16.6± 2.7 g). This led to a decrease in the ratio of shortening/force (from 100 to 14.8± 2.5% and 28.2± 6.4%). Dyskinesis produced by BDM and ischemia reperfusion was also manifested by elevated end-diastolic length (EDL), prolonged delay to shortening, systolic bulge, elevated end-shortening time delay, and tail work ratio. In contrast, intracoronay acetylcholine produced a similar decrease in both force (from 11.1± 1.3 to 7.4± 1.4 g) and muscle shortening (from 17.1± 1.5 to 9.3± 1.6%); and dobutamine caused comparable increases in both force (from 11.1± 1.3 to 20.0± 3.6 g) and shortening (from 17.1± 1.5 to 24.0± 3.1%). The ratio of shortening/force was relatively unchanged. It is concluded that uncoupling of force/shortening may produce regional dysfunction, even in the presence of normal contractility. Thus, assessment of wall motion alone may not always be an accurate estimation of myocardial contractile mechanisms.