Venous pressures and cardiac filling in turtles during apnoea and intermittent ventilation.

The amount of blood pumped by the heart (cardiac output) must be matched to the amount of blood returning to the heart (venous return), but the factors determining cardiac filling are sparsely understood in ectothermic vertebrates. Stroke volume is affected by heart rate along with central and peripheral venous pressures. In the present study, we investigated the heart rate dependency of cardiac filling in turtles, along with the changes in venous pressures that accompany ventilation. Experimental reductions in heart rate of anaesthetised turtles (Trachemys scripta) by the specific bradycardic agent zatebradine (2-3 mg kg-1) resulted in an elevation of stroke volume that compensated cardiac output. By contrast, in spontaneously ventilating turtles, stroke volume remained constant, even during the transitions from the pronounced bradycardia during breath-hold diving to the accelerated heart rate associated with spontaneous ventilation. Ventilation was associated with pronounced decreases in visceral, pericardial and central venous pressure, all of which became sub-ambient (especially during inspiration) and may provide a powerful 'suctional' element to cardiac filling. In addition, mean circulatory filling pressure, an index of vascular capacitance and the peripheral driving pressure for venous return, was increased by infusion of adrenaline (2.5 µg kg-1). Together these data demonstrate that changes in both central and peripheral venous pressures are key determinants of venous return that, in concert with direct regulation of the heart, contribute to the large scope for cardiac output in turtles.