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Intrinsic autoregulation of cardiac output in rainbow trout (Oncorhynchus mykiss) at different heart rates

SUMMARY Intrinsic regulation of the heart in teleosts is partly driven by central venous pressure, which exerts a modulatory role on stroke volume according to the well-known Frank-Starling mechanism. Although this mechanism is well understood from heart perfusion studies, less is known about how this mechanism operates in vivo, where heart rate varies markedly. We used zatebradine, a bradycardic agent, to attain resting heart rates in surgically instrumented animals. A dose of zatebradine of 2.79±0.47 mg l-1 decreased heart rate by half, from 44.4±4.19 beats min-1 to 22.1±1.9 beats min-1. Zatebradine had no significant effect on the peripheral vasculature and no inotropic effects, so was a suitable pharmacological agent with which to manipulate heart rate. When heart rate halved, cardiac output dropped to 87.5±4.6% of the control value, due to the concomitant increase in stroke volume to 165±13%. In vivo recordings of venous pressure at varying heart rates indicated that the partial compensation in cardiac output was possible through an increase in pressure in the sinus venosus, from -0.06±0.04 kPa at a control heart rate of 58.3±3.5 beats min-1 (N=10) to 0.07±0.05 kPa after injection of zatebradine (4 mg kg-1). The operation of the so-called time-dependent autoregulatory mechanism was further demonstrated in perfused hearts. The positive pressures recorded in the sinus venosus at low heart rates coincident with non-invasive measurements in trout suggest that atrial filling in trout is more dependent on the build-up of pressure in the venous circulation (vis-à-tergo filling) than a suction mechanism during ventricular contraction (vis-à-fronte filling).