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Elevated pericardial pressure and cardiac output in the leopard shark triakis semifasciata during exercise the role of the pericardioperitoneal canal



Elevated pericardial pressure and cardiac output in the leopard shark triakis semifasciata during exercise the role of the pericardioperitoneal canal



Journal of Experimental Biology 147: 263-278



Changes in pericardial pressure, pericardial fluid volume, cardiac stroke volume and heart rate induced by swimming were monitored for Triakis semifasciata (Girard). Maximum pericardial pressure (Pmax, 0.07.+-.0.03 kPa) in resting sharks was typically above ambient, whereas minimum pressure (Pmin, -0.08.+-.0.03 kPa) was slightly subambient. During swimming, both Pmax (0.23.+-.0.03 kPa) and Pmin (-0.02.+-.0.03 kPa) became elevated, as did heart rate (51.+-.2 to 55.+-.2 beats min-1) and fractional cardiac stroke volume (0.49.+-.0.03 to 0.65.+-.0.04 ml). After swimming, all variables fell, except fractional cardiac stroke volume. Estimates of total cardia output from fractional cardiac stroke volume data during rest, exercise and recovery were 33.1, 56.2 and 60.4 ml kg-1 min-1, respectively. The occurrence of both elevated pericardial pressure and cardiac output during swimming argues against a primary role for pericardial-induced vis a fronte filling as the principal mechanism responsible for increasing cardiac output withe exercise. Pericardial fluid loss via the pericardioperitoneal canal (PPC) occurs during swimming as a result of steady-state elevation of pericardial pressure, a series of transient high pericardial pressures, or both. Good general agreement seen for net pericardial fluid loss (0.6 ml kg-1) and the net increases in cardiac stroke volume (0.45 ml kg-1) during swimming establishes fluid displacement as a mechanism for increasing cardiac stroke volume and suggests that this is the primary function of the PPC.

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