High temperature and hyperkalemia cause exit block of action potentials at the atrioventricular junction of rainbow trout (Oncorhynchus mykiss) heart

• Published in: Journal of thermal biology Vol. 110; p. 103378
• Main Authors: Kuzmin, Vladislav, Ushenin, Konstantin S., Dzhumaniiazova, Irina V., Abramochkin, Denis, Vornanen, Matti
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.12.2022
• Subjects: Action Potentials; Animals; Atrioventricular delay; Bradycardia; Conduction block; Electrical excitation; Hot Temperature - adverse effects; Hyperkalemia - complications; Hyperkalemia - veterinary; Oncorhynchus mykiss; Temperature tolerance; Conduction block; Bradycardia; Electrical excitation; Atrioventricular delay; Temperature tolerance
• ISSN: 0306-4565; 1879-0992
• DOI: 10.1016/j.jtherbio.2022.103378

At critically high temperatures, atrioventricular (AV) block causes ventricular bradycardia and collapse of cardiac output in fish. Here, the possible role of the AV canal in high temperature-induced heart failure was examined. To this end, optical mapping was used to measure action potential (AP) conduction in isolated AV junction preparations of the rainbow trout (Oncorhynchus mykiss) heart during acute warming/cooling in the presence of 4 or 8 mM external K+ concentration. The preparation included the AV canal and some atrial and ventricular tissue at its edges, and it was paced either from atrial or ventricular side at a frequency of 0.67 Hz (40 beats min−1) to trigger forward (anterograde) and backward (retrograde) conduction, respectively. The propagation of AP was fast in atrial and ventricular tissues, but much slower in the AV canal, causing an AV delay. Acute warming from 15 °C to 27 °C or cooling from 15 °C to 5 °C did not impair AP conduction in the AV canal, as both anterograde and retrograde excitations propagated regularly through the AV canal. In contrast, anterograde conduction through the AV canal did not trigger ventricular excitation at the boundary zone between the AV canal and the ventricle when extracellular K+ concentration was raised from 4 mM to 8 mM at 27 °C. Also, the retrograde conduction was blocked at the border between the AV canal and the atrium in high K+ at 27 °C. These findings suggest that the AV canal is resistant against high temperatures (and high K+), but the ventricular muscle cannot be excited by APs coming from the AV canal when temperature and external K+ concentration are simultaneously elevated. Therefore, bradycardia at high temperatures in fish may occur due to inability of AP of the AV canal to trigger ventricular AP at the junctional zone between the AV canal and the proximal part of the ventricle. •The mechanisms of hyperthermia-induced loss of the ventricle contractions in fishes still not elucidated.•The role of atrioventricular (AV) canal in high temperature-induced heart failure was examined with usage of optical mapping.•Acute warming affects AP conduction in the boundary zone between the AV canal and the ventricular or atrial myocardium.•Acute warming causes conduction blocks in the boundary zones when the extracellular K+ is elevated.•The loss of ventricular functioning at high temperatures in fish occurs due to AV “exit block” facilitated by hyperkalemia.