Abstract
Isolated preparations of mammalian cardiac muscle have been employed to study possible mechanisms responsible for changes in diastolic compliance. Muscles have been studied at rest and during isometric and afterloaded contractions, at fixed initial length and during programmed, cyclic changes in length, and under the influence of paired stimulation, catecholamines, and elevated extracellular calcium concentrations. The results obtained indicate that, although there is a series viscous element in cardiac muscle, which accounts for stress-relaxation, some changes in compliance apparently result from alterations in the extensibility of the contractile element. This conclusion is based primarily on experiments showing shifts in the apex of the length-tension curve produced by action of inotropic agents which alter diastolic compliance and on experiments showing that the rate and extent of relaxation of afterloaded contractions depend on the extent of shortening during contraction.
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