Is the teleost heart oxygen limited? – Insights using “hyperoxic” incubations of contracting cardiac tissue from rainbow trout

Abstract

Considerable effort has been devoted to understanding the negative effects of reduced PO2 on cardiac function. Much less is known about the impacts of elevated PO2 (hyperoxia) on cardiac performance and energetics, especially in fishes. The fish heart is of particular interest because cardiac dependence on oxygen is extremely variable between species and the early evolution of fish occurred when atmospheric PO2 was higher than current conditions. Although extracellular PO2 is variable and normally does not exceed 21 kPa, recent evidence suggests that teleost cardiac function is stimulated at supraphysiological PO2 values. The purpose of this study was to address whether cardiac contractility and energy metabolism is responsive to elevated PO2 values in sexually-immature female rainbow trout. Isometric force development (contractility) and oxygen consumption (V̇O2) were recorded in electrically-paced ventricular preparations. Contractility and V̇O2decreased when superfusate PO2 was decreased from ~70 kPa to 57 kPa or 45 kPa. However, PO2 calculated at the preparation core was always above 18 kPa. This estimate, along with complete recovery of contractility and V̇O2 at ~70 kPa, suggests that decreases observed in cardiac performance were not due to tissue hypoxia at the lower PO2 levels. In conclusion, the heart of female rainbow trout may be oxygen-limited in vitro and this study raises new questions about the choice of appropriate PO2 for experimentation, the relevance of elevated and varying PO2 to measurements of cardiac performance, and the possible existence of an oxygen sensor within rainbow trout cardiomyocytes.