In spite of the well established negative inotropic effect (i.e., reduction of contractility) of hypercapnia on fish myocardium in vitro (seeFarrell and Jones[1992] for review), in vivo cardiac responses to hypercapnia vary among fishes, and so do the blood pressure responses (see Perry and Gilmour[2002] for a review). Obviously, in vivo cardiovascular responses to hypercapnia vary with the severity as well as the duration of hypercapnia imposed on the fish, let alone interspecific variability, and probably the experimental temperature. We have recently shown that cardiac output (blood volume pumped per unit time) decreased rapidly when yellowtail was exposed to a lethal level of hypercapnia (seawater equilibrated with a gas mixture containing 5% CO2
(Figure 3)). Heart rate did not change during the CO2 exposure, and it was a reduction of the stroke volume (blood volume pumped per contraction) that caused a reduction in cardiac output. Cardiac output began to fall before blood pressure started to rise [Lee et al., 2003]. The high solubility of CO2 will quickly lower intracellular pH of the myocardium, reducing contractility through an antagonism between hydrogen ions and intracellular calcium ions [Gesser and Poupa, 1983]. Therefore