We developed and validated a surgical technique to measure central venous pressure (CVP) in Nile tilapia, and investigated the effects of an acute temperature decrease (from 30 vs. 24 °C) and changes in heart rate (fH) using zatebradine hydrocholoride, which decreases intrinsic fH, on this species’ cardiac function. As predicted, fH and cardiac output ( \(\dot{Q}\) ) were ~ 40% lower in the acutely cooled fish, and both groups had very comparable (i.e., within 10%) values for stroke volume (VS). The CVP of fish acutely exposed to 24 °C was consistently ~ 0.04 kPa higher than in those measured at 30 °C across all concentrations of zatebradine (i.e., CVP increased from 0.04 to 0.11 kPa vs. − 0.01–0.07 kPa for 24 vs. 30 °C tilapia, respectively, as fH was reduced). However, this did not result in an increase in VS due to a right-shifted relationship between CVP and VS for the 24 °C fish. These data suggest that the VS of tilapia is less sensitive to changes/increases in CVP when temperature is acutely lowered, and that regardless of increases in preload (CVP), \(\dot{Q}\) is primarily modulated by fH in this species.
