Diastolic scattered light fluctuation, resting force and twitch force in mammalian cardiac muscle.

1. When coherent light was passed through isolated isometric cardiac muscles during the diastolic or resting period, intensity fluctuations were observed in the scattered field. The frequency of these intensity fluctuations (f((1/2))) varied with many experimental interventions known to enhance Ca(2+) flux into the cell.2. In rat muscles stimulated at low frequencies (0.1 +/- 2.0 min(-1)) stepwise increases (0.4-10 mm) of [Ca(2+)] in the bathing fluid ([Ca(2+)](e)), or addition of ouabain (10(-6)-6 x 10(-4)m) to the perfusate caused stepwise increases in f((1/2)). These were paralleled by increments in resting force (RF) such that the changes in f((1/2)) and RF were highly correlated. Substitution of K(+) for Na(+) in the perfusate resulted in parallel transients in RF and f((1/2)).3. In contrast to the rat, most cat muscles stimulated at low frequencies in the steady state exhibited neither diastolic intensity fluctuations nor Ca(2+)-dependent changes in RF in [Ca(2+)](e) of 10 mm or less; when [Ca(2+)](e) was increased to 12-32 mm, however, steady-state Ca(2+)-dependent f((1/2)) and RF were observed. In a given [Ca(2+)](e) reduction of [Na(+)](e) increased f((1/2)). In the transient state following cessation of regular stimulation at more rapid rates (12-96 min(-1)) intensity fluctuations were present in all [Ca(2+)](e) and decayed with time (seconds to minutes); the f((1/2)) and time course of the decay of the fluctuations were determined by the rate of prior stimulation and [Ca(2+)](e).4. Maximum potentiation of twitch force in response to the above inotropic interventions was associated with an optimal level of f((1/2)) which was similar in both species; when higher levels of f((1/2)) were produced by more intense inotropic intervention, twitch force declined. Over the range of inotropic intervention up to and including that at which maximum twitch potentiation occurred, the increase in diastolic f((1/2)) predicted the extent of twitch potentiation with a high degree of accuracy (r > 0.97) both in the transient and steady states.5. In contrast to the other inotropic interventions studied, catecholamines were unique in that neither f((1/2)) nor RF increased over a full range of concentrations that resulted in maximum potentiation of the twitch.6. It is concluded from these observations that f((1/2)) reflects diastolic Ca(2+)-dependent myofilament interaction; the increase in the extent of this interaction by inotropic interventions that do not alter the affinity of the myofilaments for Ca(2+) probably reflects an increase in diastolic myoplasmic [Ca(2+)], an optimal level of which is associated with maximal potentiation of twitch force; the difference in f((1/2)) in rat and cat muscles under a given set of in vitro conditions may be related to the marked species difference in the effectiveness of excitation-contraction coupling.