Elevated Pericardial Pressure And Cardiac Output In The Leopard Shark Triakis Semifasciata During Exercise: The Role Of The Pericardioperitoneal Canal

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±0.04ml). After swimming, all variables fell, except fractional cardiac stroke volume. Estimates of total cardiac 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 with 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−) and the net increase in cardiac stroke volume (0.45 ml kg−) during swimming establishes fluid displacement as a mechanism for increasing cardiac stroke volume and suggests that this is the primary function of the PPC.

Function of the pericardium and pericardioperitoneal canal in elasmobranch fishes

Previous studies of cardiac function in elasmobranch fishes have not included the influence of the pericardioperitoneal canal on pericardial pressure and volume and thus on cardiac function. Accordingly, we studied the function of the pericardium and pericardioperitoneal canal in sharks and rays. We found negative pericardial pressure that rose to a plateau of approximately 0 mmHg when fluid was infused into the pericardium with the canal undisturbed. However, this pericardial pressure elevation caused severe cardiac tamponade. After the canal was occluded, the pressure plateau was substituted with an exponential rise. We injected radioisotopes into the pericardial cavity and obtained scintigrams several hours later. The scans and counts of body fluids and tissues indicated absorption, disputing the suggestion that the primary function of the canal may be inadequate absorption of pericardial fluid. We conclude that the pericardioperitoneal canal maintains negative pericardial pressure, which is a prerequisite in elasmobranch fishes and may serve to regulate pericardial pressure level to optimize cardiac function in relation to changes in cardiac size.