Nonuniformity of sarcomere shortenings in the isolated rat ventricular myocyte

By projecting the image of a single ventricular myocyte upon a linear image sensor, the striation pattern was analyzed during resting and contracting states. During rest, the individual cycle length (ICL) of the striation pattern varied from 1.8 to 2.0 microm within a given cell. ICL measured every 2 ms fluctuated approximately 0.05 microm around the mean. The variance of temporal fluctuations was decreased by chelating the extracellular Ca(2+) and increased by the Ca(2+) overload. Blocking the Ca(2+) release channels with 10 micromol/l ryanodine reversed this increase. In the power spectral density, an increase in the power occurred in the frequency range below 10 Hz. This increase should reflect overall kinetics of both intracellular Ca(2+) handling and responses of contractile filaments, because the same pattern was observed when spontaneous contractions occurred as well as when contractions were evoked by activating the L-type Ca(2+) channels. It is suggested that the temporal fluctuations of ICL in the resting state are caused by spontaneous Ca(2+) release from ryanodine receptors on the sarcoplasmic reticulum. Furthermore, under evoked contractions the shortenings of ICL were spatially inhomogeneous. These findings of nonuniform sarcomere shortenings are consistent with the temporal and spatial inhomogeneity of Ca(2+) transients.