Physiologic aspects of relaxation of the myocardium.

To understand relaxation in the intact heart, an appreciation of myocardial relaxation in controlled isometric and isotonic twitches is a prerequisite. Load dependence of myocardial relaxation is manifest as the temporal separation of relaxation in isotonic and isometric twitches, i.e. rapid isotonic lengthening in contrast to slower isometric force decline. Although both isotonic and isometric relaxation modes are governed by the same determinants of crossbridge kinetics (life cycle of individual crossbridges along with regulatory properties of the contractile proteins, and calcium sequestration particularly by the sarcoplasmic reticulum), the contribution of these determinants in controlling onset and rate of relaxation is different in isometric force decline and in isotonic lengthening. In an isometric twitch, cooperative activity will, through a process of force development-induced increased sensitivity of the contractile proteins, upgrade the development and maintenance of force throughout contraction and relaxation. On the other hand, a functional calcium sequestration by the sarcoplasmic reticulum will, in the presence of a reduced effect of cooperative activity in the isotonic twitch, allow for load-induced rapid lengthening. Marked mechanical nonuniformity is observed in intact cardiac muscle. Nonuniformity in cardiac muscle mechanics is usually considered as a nuisance. Uniform behaviour of overall muscle does occur, however, despite or perhaps through nonuniform behaviour of longitudinal muscle segments. A limited but variable degree of nonuniformity therefore probably constitutes an essential property of the heart. A quantitative analysis of nonuniformity in isolated cat papillary muscle is proposed. Pathological considerations require extrapolation of our understanding from isolated muscle relaxation to ventricular relaxation.(ABSTRACT TRUNCATED AT 250 WORDS)