Rapid Relengthening in Isolated Cardiac Cells and the Origin of Diastolic Recoil
Late relengthening in both intact muscle and in the isolated cardiac muscle cell is characterised by two distinct phases that represent separate intracellular compartments or steps in the relaxation process. The rapidity of the first component facilitates the rapid relaxation that is required to promote early filling of the heart. Conversely, early filling will be slowed by any factor that increases loading or sarcomere length. Late diastolic properties in normal myocardium represent an independent mechanism which probably reflects extrusion of calcium ion from the cell rather than its reuptake by the intracellular compartments. The magnitude of just one internal restoring force in the single cell can be estimated to be on the order of 0.2–0.4 mN/mm2. This value probably represents a lower limit to the true intracellular restoring force, and it is not known whether the cell lengthens in a truly elastic fashion. Application of a simple model of the ventricle indicates that, even at this minimal level, the cellular restoring force would account for a negative pressure of ∼ 10mmHg. Thus the actual magnitude of the negative pressures developed during early filling in the myocardium is largely consistent with the component which originates by lengthening of the isolated cell. The true restoring force that arises in the cell may be much larger, and it is worth considering the possibility that extracellular structures counteract the cellular restoring force. The quantitative parallel between cellular and myocadial restoring forces does not exclude the extracellular matrix as a restoring force between layers of the heart but, for the moment, the predictions based on a role for the elastic distortion of the latter are not easy to reconcile with the mechanics of the isolated muscle.
KeywordsWall Stress Sarcomere Length Cardiac Muscle Cell Early Filling Unattached Cell
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