In fish, catecholamine-induced changes in cardiac performance in vivo are the result of complex interactions between the direct adrenergic effects on the heart and peripheral circulation and the reflex responses to increased blood pressure. In addition, coronary artery transport of catecholamines and oxygen to the compact myocardium may be essential for maximal in vivo cardiac performance during adrenergic stimulation. Cardiac output (Q(dot)), heart rate (fh), stroke volume (Vs) and dorsal aortic pressure (Pda) were measured in trout with intact or ablated coronary arteries at rest and following intra-arterial administration of 0.2, 0.5, 1.0 and 2.0 µg kg-1 adrenaline. Resting Q(dot), fh, Vs and Pda were the same in fish with intact and ablated coronaries at 48 h post-surgery, averaging approximately 18 ml min-1 kg-1, 42 beats min-1, 0.42 ml kg-1 and 2.2 kPa, respectively. All cardiovascular variables showed a strong relationship between response magnitude and adrenaline dose. However, our results indicate that adrenaline doses above 0.5 µg kg-1 may have a limited ability to increase Q(dot) (ED50 0.22 µg kg-1). Coronary artery ablation had little effect on post-injection Q(dot), Vs, Pda or fh at any dose of adrenaline. In both intact and ablated groups, two types of responses in Q(dot) were observed following adrenaline injection. In the ‘type 1′ response, Q(dot) increased shortly (15–30 s) after adrenaline administration, as increases in Vs more than compensated for a pressor-stimulated reflex bradycardia. In the ‘type 2′ response, alterations in Q(dot) were biphasic. In the initial minutes post-injection, Q(dot) fell and reached a minimum level at 1–2 min, the result of an immediate drop in fh and a delayed post-injection increase in Vs. Thereafter, Q(dot) gradually increased as a result of concordant increases in fh and Vs. Although time to maximum Q(dot) was 5–6 min longer for fish exhibiting type 2 responses, there was no difference in maximum Q(dot) increase or in the time courses for changes in fh and Pda between response types. Our results suggest (1) that during normoxic conditions, cardiac performance does not depend highly on coronary blood flow; (2) that the capacity of adrenaline to increase Q(dot) may be limited by elevations in output pressure and/or by the low dose (concentration) of adrenaline required to achieve near maximal adrenergic stimulation of the heart; and (3) that fish exhibiting type 2 responses have an increased barostatic gain (%delta fh per unit Pda) compared with those with type 1 responses.

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