Role of venoconstriction in the cardiovascular responses of ducks to head immersion

Abstract

Central venous pressure of ducks rose from resting values of 0.31 +/- 0.16 (SE) to 1.75 +/- 0.20 kPa during forced head immersion. Because a similar increase in mean circulatory pressure (Pmc) was also observed (0.71 +/- 0.16 to 2.15 +/- 0.20 kPa) the rise in central venous pressure was attributed to a venoconstrictor mechanism. When this venoconstrictor-induced rise in central venous pressure was prevented by graded withdrawal of venous blood, then immersion bradycardia was inhibited, and the reduced cardiac output associated with head immersion was largely the result of reduced stroke volume. When compared with normal dives, this intervention resulted in greater myocardial energy requirements, as assessed by the pressure-rate product. It is concluded that venoconstriction increases central venous pressure during head immersion. The increase in central venous pressure alters cardiac function through the Frank-Starling mechanism such that myocardial energy requirements are minimized during this period of low oxygen availability.