Jaakko Haverinen and Matti Vornanen
At critically high temperature, cardiac output in fish collapses as a result of depression of heart rate (bradycardia). However, the cause of bradycardia remains unresolved. To investigate this, rainbow trout (Oncorhynchus mykiss; acclimated at 12°C) were exposed to acute warming while electrocardiograms were recorded. From 12°C to 25.3°C, electrical excitation between different parts of the heart was coordinated, but above 25.3°C, atrial and ventricular beating rates became partly dissociated because of 2:1 atrioventricular (AV) block. With further warming, atrial rate increased to a peak value of 188±22 beats min–1 at 27°C, whereas the ventricle rate peaked at 124±10 beats min–1 at 25.3°C and thereafter dropped to 111±15 beats min–1 at 27°C. In single ventricular myocytes, warming from 12°C to 25°C attenuated electrical excitability as evidenced by increases in rheobase current and the size of critical depolarization required to trigger action potential. 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 owing to the increased excitation threshold of the ventricle, which is due to changes in the 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 cardiac function in vivo provides a mechanistic explanation for the depression of cardiac output in fish at critically high temperature.