4.5 Article

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

期刊

JOURNAL OF THERMAL BIOLOGY
卷 110, 期 -, 页码 -

出版社

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.jtherbio.2022.103378

关键词

Electrical excitation; Atrioventricular delay; Bradycardia; Conduction block; Temperature tolerance

资金

  1. Academy of Finland [15051]
  2. Interdisciplinary Scientific and Educational School of Moscow University Molecular Technologies of the Living Systems and Synthetic Biology
  3. Russian Ministry of Science and Higher Education [122012100156-5]

向作者/读者索取更多资源

This study investigates the role of the atrioventricular (AV) canal in high temperature-induced heart failure in fish. The results show that the AV canal is resistant to high temperatures and high external K+ concentrations, but it is unable to trigger ventricular excitation when both temperature and external K+ concentration are elevated. This finding sheds light on the mechanism of bradycardia at high temperatures in fish.
At critically high temperatures, atrioventricular (AV) block causes ventricular bradycardia and collapse of car-diac 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 propa-gation of AP was fast in atrial and ventricular tissues, but much slower in the AV canal, causing an AV delay. Acute warming from 15 degrees C to 27 degrees C or cooling from 15 degrees C to 5 degrees C did not impair AP conduction in the AV canal, as both anterograde and retrograde excitations propagated regularly through the AV canal. In contrast, anter-ograde 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 degrees C. Also, the retrograde conduction was blocked at the border between the AV canal and the atrium in high K+ at 27 degrees 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.

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