Calcium-dependent mechanical oscillations occur spontaneously in unstimulated mammalian cardiac tissues.

Abstract

In quiescent rat ventricular myocardium, bathed in solution of 2 mM Ca++ or less, it has been previously demonstrated that spontaneous microscopic oscillatory cell motion is present and interacts with an incident laser beam to produce scattered light intensity fluctuations which can be monitored to quantify the underlying motion. The present study shows that scattered light intensity fluctuations are not present under any conditions in frog atrial or ventricular preparations, but do occur in each type of mammalian cardiac tissue studied in the unstimulated state. The magnitude of scattered light intensity fluctuations in mammalian tissues varies with species and cellular Ca++ loading. In some tissues, e.g., rabbit or ferret ventricle, either an increase in the Ca++ concentration in the perfusate [( Ca++]e), reduction of perfusate Na+ concentration [( Na+]e), or addition of cardiac glycosides was required to elicit scattered light intensity fluctuations; in other tissues, however, e.g., the canine Purkinje fiber, atria, and ventricle, and guinea pig atria, scattered light intensity fluctuations were present at 2 mM [Ca++]e in the absence of experimental Ca++ loading. Scattered light intensity fluctuations were not affected by LaCl3, or verapamil, and were reversibly abolished by caffeine. When the pCa in the myofilament space is kept constant in detergent "skinned" fibers, scattered light intensity fluctuations are not present during contractile activation. We conclude: that scattered light intensity fluctuations are due to spontaneous intracellular Ca++ oscillations that require a functional sarcoplasmic reticulum; that the potential to exhibit these oscillations is a fundamental property of mammalian excitable cardiac cells; and that, in many mammalian tissues, these oscillations are present in the unstimulated state, even in the absence of experimental perturbations to enhance cell Ca++ loading.

Calcium oscillations index the extent of calcium loading and predict functional recovery during reperfusion in rat myocardium.

“…These data further support the notion that excessive SLIF during reflow, at a time when pH, inorganic phosphate, and high-energy phosphates are constant, reflects the occurrence of cell calcium overload. The results of additional protocols in the same experimental model in the present study and in previous studies (19)(20)(21) (16,(19)(20)(21) in the subsequent systole. In addition, spontaneous diastolic sarcoplasmic reticulum calcium release could result in less action potential-generated calcium flux in the subsequent systole because of calcium-dependent inactivation of L-type calcium currents.…”

“…In addition, spontaneous diastolic sarcoplasmic reticulum calcium release could result in less action potential-generated calcium flux in the subsequent systole because of calcium-dependent inactivation of L-type calcium currents. Finally the areas throughout the tissue where there is reduced calcium release will act as compliant "islands" diminishing the tension the total muscle will develop (16 (36). In the present study, developed pressure at the end of the reperfusion period was improved in the group receiving low calcium during early reperfusion, recovering to a mean of 74% of its initial value.…”

“…To study the significance of these factors during early the postischemic recovery period, phosphorus-3 1 nuclear vasively and repetitively quantify high-energy phosphates (ATP and phosphocreatine [PCr]), inorganic phosphate (Pi), and intracellular pH (13) and spectroscopy of scattered laser light was used to study spontaneous diastolic sarcoplasmic reticulum-myofilament calcium oscillations (14,15). Spontaneous, asynchronous, myocardial calcium oscillations, which do not require membrane depolarization, have been shown to occur in various cardiac preparations in mammalian species (16,17). These have been attributed to calcium-dependent calcium release from the sarcoplasmic reticulum and exhibit a periodicity which depends on cell calcium loading (18).…”

Cardiac Basal Metabolism.

“…This notion, inferred by Nayler and colleagues [154,155] from direct measurements of uptake and retention of Ca 2ϩ by cardiac microsomes, was used by Gibbs and Loiselle [100] to explain a species difference in activation heat. This same species-difference (ratϾguinea pig) was suggested by a series of papers from the laboratory of Lakatta [156][157][158][159][160][161] in which the occurrence of spontaneous light intensity and mechanical fluctuations were attributed to spontaneous release of Ca 2ϩ from the SR under resting conditions. More recently, the discovery of Ca 2ϩ -sparks, using techniques of laser-scanning confocal microscopy, has further legitimized the phenomenon of spontaneous Ca 2ϩ release from the sarcoplasmic reticulum [162][163][164][165][166][167][168][169][170][171].…”

2APB- and JTV519(K201)-sensitive micro Ca2+ waves in arrhythmogenic Purkinje cells that survive in infarcted canine heart

“…Subsequently, spontaneous contractions, spontaneous oscillations in both current and potential, were described in both multicellular and myocyte preparations. 33 - 35 The amplitude of spontaneous Ca 2+ oscillations depends on the level of intracellular Ca 2+ much like the triggered oscillations in Ca i that have been shown to be concomitant with delayed afterdepolarizations. 36 -38 Thus, spontaneous Ca 2+ oscillations are not due to transmembrane potential changes but, given the correct initiating conditions, cause traveling Ca 2+ waves, depolarizations, and nondriven action potentials.…”