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At critically high temperature, cardiac output in fish collapses due to depression of heart rate (bradycardia). However, the cause of bradycardia remains unresolved. To this end rainbow trout (Oncorhynchus mykiss; acclimated at +12°C) were exposed to acute warming, while electrocardiograms were recorded. From +12℃ to +25.3℃, electrical excitation between different parts of the heart was coordinated but above +25.3℃ atrial and ventricular beating rates became partly dissociated due to 2:1 atrioventricular (AV) block. With further warming atrial rate increased to the peak value of 188±22 bpm at +27℃, while the rate of the ventricle reached the peak value of 124±10 bpm at +25.3 ℃ and thereafter dropped to 111±15 bpm at +27℃. In single ventricular myocytes, warming from +12°C to +25°C attenuated electrical excitability as evidenced by increases in rheobase current and critical depolarization required to trigger action potential. The depression of excitability was caused by temperature induced decrease in input resistance (sarcolemmal K+ leak via the outward IK1 current) of resting myocytes and decrease in inward charge transfer by the Na+ current (INa) of active myocytes. Collectively these findings show that at critically high temperatures AV block causes ventricular bradycardia which is an outcome from the increased excitation threshold of the ventricle due to changes in passive (resting ion leak) and active (inward charge movement) electrical properties of ventricular myocytes. The sequence of events from the level of ion channels to the cardiac function in vivo provides a mechanistic explanation for the depression of cardiac output in fish at critically high temperature.

Atrioventricular block, due to reduced ventricular excitability, causes the depression of fish heart rate in fish at critically high temperatures