It is widely recognized that calcium is of singular importance in the viability of the myocardial cell, nonetheless little is known concerning the precise nature of the action of calcium in myocardium as to how it maintains the life of the cell and how it may dictate the death of the cell. However, recent advances in research involved with the study of calcium movement in the heart have been highly valuable for the formulation of new concepts with respect to the physiological and pathological aspects of calcium metabolism in the myocardium. It is becoming clear that calcium movements are closely related to cardiac electrophysiological events, contractile function, membrane integrity and energy metabolism. In particular, a novel theory involving phosphatidylinositol turnover and Ca2+-dependent ATPase activation has been advanced regarding the mechanism and control of calcium entry into the cardiac cell upon excitation. Alterations in the regulation of calcium metabolism through the interaction of a number of separate, elements may affect calcium distribution in the cell and thereby may change cardiac function and metabolism. The part calcium plays in the genesis of pathological states in the myocardium is discussed in the light of research employing various experimental protocols. Intracellular calcium overload and deficiency are postulated to contribute to cardiac contractile failure and cell death through a number of distinct mechanisms. It is now a real challenge to understand the precise nature of processes associated with the occurrence of intracellular calcium overload or intracellular calcium deficiency in order to achieve proper management of cardiac disorders.

Calcium movements in relation to heart function.

Routine hemodialysis is associated with an increase in left ventricular contractility that is independent of a change in preload, but the mechanisms responsible are unknown. We investigated the importance of three distinct effects that regularly occur in hemodialysis and could potentially improve left ventricular contractility: the removal of uremic toxins, the increase in the plasma ionized calcium concentration, and the increase in the plasma bicarbonate concentration. Three different dialysates were used for each of eight stable patients on long-term hemodialysis, and left ventricular contractility was assessed by two-dimensional echocardiography before and after each dialysis. In the first procedure neither the ionized calcium nor the bicarbonate concentration was allowed to increase, and left ventricular contractility did not improve. In the second procedure, ionized calcium increased (from 4.4 to 5.4 mg per deciliter, P<0.001), bicarbonate concentration was held constant, and contractility ...

Increased ionized calcium and left ventricular contractility during hemodialysis.

Study Objective:To determine the effect of variations in blood ionized calcium (Ca2+) on myocardial contractility independent of changes in loading conditions and other biochemical variabl...

Left Ventricular Contractility Varies Directly with Blood Ionized Calcium

Ca2+-induced Ca2+ release at the terminal cisternae of skeletal sarcoplasmic reticulum was demonstrated using heavy sarcoplasmic reticulum vesicles. Ca2+ release was observed at 10 μm Ca2+ in the presence of 1.25mm free Mg2+ and was sensitive to low concentrations of ruthenium red and was partially inhibited by valinomycin. These results suggest that the Ca2+-induced Ca2+ release is electrogenic and that an inside negative membrane potential created by the Ca2+ flux opens a second channel that releases Ca2+. Results in support of this formulation were obtained by applying a Cl− gradient or K+ gradient to sarcoplasmic reticulum vesicles to initiate Ca2+ release. Based on experiments the following hypothesis for the excitation-contraction coupling of skeletal muscle was formulated. On excitation, small amounts of Ca2+ enter from the transverse tubule and interact with a Ca2+ receptor at the terminal cisternae and cause Ca2+ release (Ca2+-induced Ca2+ release). This Ca2+ flux generates an inside negative membrane potential which opens voltage-gated Ca2+ channels (membrane potential-dependent Ca2+ release) in amounts sufficient for contraction.

Mechanism of calcium release from skeletal sarcoplasmic reticulum

Prior to consideration of the effects of digitalis compounds on ionic exchange the basic mechanisms of active Na+ and K+ transport are discussed. It is generally accepted that digitalis is a specific inhibitor of the Na+-K+ activated ATPase located primarily in the sarcolemmal membrane. Present evidence supports the concept that positive inotropic effects of digitalis are not seen unless evidence of inhibition of the enzyme and, therefore, of the "Na pump" leads to a small increase of intracellular Na+. This leads to augmented activity of a Na+ transport system which is coupled, not to K+, but to Ca+ +. Evidence for the existence of Na+-Ca+ + coupling at excitable membranes is accumulating, and this is reviewed. The possibility that administration of digitalis, through its inhibition of the Na+-K+ coupled system produces an increase in Na+- Ca+ + coupled transport and thereby an increase of influx of Ca+ + to the myofilaments is discussed and is presented as a possible basis for the mechanism of digitalis...

Effects of digitalis on myocardial ionic exchange.

The relationship between cellular calcium (Ca) stores and isometric contractile force was investigated in isolated, gas-perfused cat hearts. The hearts were preperfused for approximately 5 min with substrate-free Krebs solution modified to contain 0, 1.25, 2.5, 5.0 or 10.0 mEq/liter Ca, gas-perfused for up to 120 min, and then perfused with zero-Ca Krebs solution. Contractile force and [Ca] in the effluent fluid were measured. Our results indicate that: (a) The washout of Ca was characteristic of a three compartment system, (b) A Ca compartment directly associated with muscle contraction was identified by correlation of the rate of Ca washout with the rate of decay of contractility (r = 0.79). (c) Ca content in the compartment was correlated with contractile force (r = 0.77). (d) Contractile force and the Ca content of the compartment which was correlated with contractility approached a steady state during 120 min of gas perfusion.

https://rupress.org/jgp/article-pdf/52/6/969/1244479/969.pdf

Correlation of contractile force with a calcium pool in the isolated cat heart.

Krebs-Henseleit solution as a physiological buffer in perfused and superfused preparations

We have investigated the effect of chlorpromazine and aldosterone on the positive inotropic effect and the subcellular distribution of 3H-digoxin in isolated, electrically driven guinea-pig hearts. Both drugs decreased the positive inotropic effect of 3H-digoxin and the uptake of the drug by the microsomal fraction, whereas the total tissue uptake and the tissue/medium ratio of the radioactivity did not differ significantly from control. Because all measurements were made in the same experiments, we were able to show a significant correlation between the positive inotropic effect and the content of 3H-digoxin in a crude microsomal fraction, but not in the mitochondrial or nuclear fractions. A significant fraction of the bound drug was released into the supernatant when the microsomal pellet was shaken in Krebs' solution and recentrifuged. There was a greater correlation of the inotropic effect with the loosely bound drug than with the total microsomal binding; there was no correlation between contractility and the drug remaining in the microsomal pellet. Gel filtration of the supernatant showed that the drug was not bound to a macromolecule. We suggest that the digoxin taken up by the cell and bound loosely to a constituent of the microsomal fraction is responsible for the positive inotropic effect.

Correlation of the subcellular distribution of digoxin with the positive inotropic effect

Es wird angenommen, dass mindestens zwei Fraktionen von intrazellularem Kalzium am Kupplungsprozess zwischen Reizung und Kontraktion des Herzens beteiligt sind

Two functionally distinct calcium pools in the excitation-contraction coupling process

The effect of insulin on the subcellular distribution and the inotropic effect of 3H-digoxin in the guinea pig heart

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