Identifies and characterizes the electrical activity of functional subsidiary pacemakers in the canine inferior right atrium, highlighting their potential to cause atrial dysrhythmias via spontaneous and triggered activity.
Glass microelectrodes were used to study the electrical activity of the subsidiary atrial pacemaker (SAP) cells that maintain atrial excitation after suppression of the sinoatrial node. Tissues with documented SAP activity were isolated from the canine inferior right atrium and superfused in vitro with Tyrode solution containing norepinephrine (NE, 10(-8)-10(-7) M). SAP action potentials exhibited prominent diastolic depolarization and a significantly lower maximum diastolic potential, take-off potential, overshoot, rate of rise, and amplitude than typical atrial muscle. Withdrawal of NE completely blocked SAP propagation, although SAP automaticity continued at a slower rate. Acetylcholine (ACh, 5 X 10(-8) M) usually produced complete exit block and decreased spontaneous rate. Higher concentrations of ACh (10(-6) M) elicited a prominent hyperpolarization (19.2 +/- 6.6 mV), completely suppressing SAP automaticity. In quiescent preparations exposed to NE greater than or equal to 10(-7) M, external stimuli at short cycle lengths (less than 1,000 ms) elicited action potentials with delayed afterdepolarizations, which frequently caused nondriven repetitive activity. This triggered activity was inhibited by verapamil or withdrawal of NE. These studies identify and characterize the electrical activity of functional subsidiary pacemakers located in a specific region of the inferior right atrium. In addition, fibers within this region display triggered activity. Spontaneous activity generated by fibers within the SAP region may cause atrial dysrhythmias.
Rozanski et al. (1985) studied this question.