Cardiovascular dynamics and adrenergic responses of the rainbow trout in vivo.

TLDR: The cardiac response reflected a varying balance between a direct beta-stimulatory effect of adrenaline on Q and an indirect passive inhibition of Q by the increase in peripheral resistance, both effects were mediated through changes in stroke volume.

Abstract: Cardiac output and dorsal aorta, ventral aorta, caudal artery, caudal vein, and subintestinal vein pressures have been directly measured in intact unanaesthetized trout. Cardiac output (Q) averaged 36.7 ml/kg.min. The pressure drop across the systemic vascular resistance (Rs) was approximately twice that across the gill resistance (Rg), and a significant positive pressure persisted in the venous system. alpha-Adrenergic blockade revealed a considerable endogenous vasomotor tone resulting from latent adrenergic constriction of Rs. Intravenous adrenaline caused a pressor response throughout the circulatory system which has been analysed in detail with the aid of previous studies on isolated parts of the trout circulation. The complex and variable form of the pressor response reflected differential contributions from changes in Q, Rg, and Rs. Increases in Rs (alpha-receptor activation) were the principal cause of all pressor responses. Rg usually declined slightly due to passive dilation and/or beta-receptor stimulation, but occasionally increased due to alpha-receptor activation. The cardiac response reflected a varying balance between a direct beta-stimulatory effect of adrenaline on Q and an indirect passive inhibition of Q by the increase in peripheral resistance. Both effects were mediated through changes in stroke volume. Occasional tachycardia or more frequent reflex bradycardia were minor components of the cardiac response. The in vivo actions of other adrenergic agents have been similarly analysed.