Di Palma, Joseph R.
August 1958
Angiology;Aug1958, Vol. 9 Issue 4, p219
Academic Journal
Two direct atrial action potentials were recorded in the anesthetized dog. One potential was made at the SA node as a monophasic current; the other was made at the area of the AV node as a diphasic current. The time of excitation of the AV node could be seen on these records. Thus the following items could be measured and observed: 1. The transmission time from the SA node to the region of the AV node. 2. Comparison of the contour of the SA monophasic potential to that of the AV diphasic potential. 3. The P-R interval. 4. The relationship of the firing of the AV node (onset of the QRS complex) to the contour of the two action potentials. It was found that normally the AV node was excited at the time of repolarization of the atrium rather than depolarization. With reference to the monophasic potential this corresponded to the change between slow and fast repolarization; with the diphasic potential excitation of the AV node occurred early in the atrial T wave. Acetylcholine or vagus stimulation caused the monophasic potential to become more triangular with corresponding changes in the diphasic potential. The time of firing of the AV node was delayed until ropolarization was completed. The SA-AV transmission time was not altered. The P-R interval was consequently lengthened. More extreme effects included a diminished amplitude of atrial action potential and failure of the AV node to be excited with the production of complete heart block. These effects on the action potentials of the atrium could be completely prevented by atropine. Epinephrine caused the atrial monophasic potential to become more square shortening the slow phase of ropolarization. This corresponded to a decreased P-R interval. These results support the experimental approach of Gilson and the latency theory of Erlanger as explanations of the delay of the cardiac impulse at the AV node. Moreover, the results with acetylcholine and epinephrine elucidated the mechanism by which the heart adjusts the AV nodal delay to changing requirements.


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