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