Effect of hypothermia on excitation and propagation in the isolated atrium

Abstract

Cooling rabbit right atria from 37 to 21 C resulted in only slight changes in excitability in contrast to a fivefold decrease in the spontaneous rate of excitation. Atrial arrest occurred at approximately 21 C and was characterized by a small nonpropagated electrical event associated with little or no tension development. In seven preparations repeatedly cooled and rewarmed no apparent relationship existed between changes in atrial excitability and either the onset of arrest or the resumption of activity subsequent to rewarming. Acetylcholine consistently restored normal electrical and mechanical activity in hypothermia-arrested atria for at least 20 min. This "excitatory" action of acetylcholine occurred independently of the existing level of atrial excitability. The continued presence of pacemaker activity and the lack of correlated changes in atrial excitability suggest that hypothermic atrial arrest is primarily the result of an impairment of sinoatrial conduction. The condition may be similar to the conduction block induced by elevated extracellular potassium.