In rainbow trout, atrial myocardium contracts faster than ventricular myocardium, and cold acclimation enhances contraction kinetics and SR calcium handling to maintain cardiac function at low temperatures.
Atrial and ventricular myocardium perform different tasks in the pumping work of the vertebrate heart, which are reflected in their contractile properties. Although atrial contraction is assumed to have an important role in the function of fish heart, the contractile properties of atrial and ventricular myocardium have not been directly compared in any fish species. The objective of this study was to clarify any contractile differences in the heart of teleost fish and, in particular, to elucidate the contribution of myofibrillar ATPase and intracellular Ca(2+) stores to the characteristics of atrial and ventricular contraction. Experiments were conducted on thermally acclimated rainbow trout Oncorhynchus mykiss to determine whether the effects of temperature adaptation are the same in atrial and ventricular tissue. It was shown that the rate of isometric contraction is much faster in atrial than in ventricular tissue of the fish heart and that acclimation to cold increases the rate of contraction in both cardiac compartments. The rapid contraction kinetics of the atrial tissue were associated with higher myofibrillar ATPase activity and faster Ca(2+) uptake rate of the sarcoplasmic reticulum (SR) compared with ventricular tissue. Similarly, the faster kinetics of contraction following cold acclimation could be attributed to enhancement of the myofibrillar and/or SR function. The atrio-ventricular and temperature-induced differences were also expressed in the recovery of force from inactivation, i.e. in the mechanical restitution. The refractory period and the rate constant of force restitution were shorter in atrial than in ventricular muscle tissue. Similar differences also existed between the tissues of cold-acclimated (CA, 4 degrees C) and warm-acclimated (WA, 17 degrees C) fish. The fast recovery of force from inactivation in the heart of the CA trout was, at least in part, due to more active SR. Furthermore, it was shown that the force of atrial contraction in the CA trout is sensitive to ryanodine (10 ()mol l(-)(1)), a Ca(2+)-release channel blocker of SR, at physiological body temperature (4 degrees C) and at a physiological pacing rate (0.6 Hz). This finding indicates that the Ca(2+) stores of SR contribute to activation of cardiac contraction in the fish heart, and that the SR of fish heart is able to retain its Ca(2+) load at low body temperatures, i.e. the Ca(2+ )release channels of SR are not leaky in the cold. The present data show that in the atrial tissue of CA trout, the SR directly contributes to the cytosolic Ca(2+) and that in the atrium and ventricle of CA trout, the SR significantly accelerates the recovery of contractility from inactivation. The fast recovery from inactivation allows relatively high heart rates and therefore adequate cardiac outputs at low environmental temperatures for the cold-active rainbow trout.
Aho et al. (Fri,) studied this question.