EXCITATION OF THE HEART 



297 



J 



630 

 500 



400 

 320 



250 

 200 



200 



160 



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^n 



■r^ 



FIG. 14. Effects of stimulation at several frequencies on A-V 

 nodal and bundle potentials. Column .1 shows a negative- 

 going A-V nodal potential which follows a large negative 

 atrial potential. The recording electrode was within the A-V 

 node. Column B illustrates potentials recorded 2 mm away, 

 near origin of common bundle. Small negative potential follow- 

 ing atrial potential in A and positive-going potential preceding 

 rapid depolarization of common bundle in B are due to activa- 

 tion of A-V node. Magnitude of A-V nodal potential in both 

 A and B can be seen by comparison with potentials recorded 

 at interstimulus interval of 160 msec, which show neither 

 A-V nodal nor bundle activity (complete block). Atrial po- 

 tentials in .4 are of 2 mv magnitude; time pips are at 20 msec. 

 [From Scher el al. (116).] 



obtained a polyphasic deflection in bipolar recordings 

 from tlie perinodal region in the dog. They felt this 

 potential was from the A-V node. Pruitt & Essex 

 (gi ), who studied the calf and dog, believe such a 

 potential at times originates from atrial fibers im- 

 mediately above the A-V node or from the atrionodal 

 junction; however, their records are generally 

 unipolar. The significance of a particular potential 

 shape in a bipolar record from the nodal region 

 appears obscure. Scher and co-workers (116), also 

 working with dogs, were unable to find in the peri- 

 nodal region any potentials of the type reported by 

 van der Kooi and co-workers. The extracellular 

 potentials recorded from the A-V node by Pruitt and 

 Essex, and by Scher and his co-workers appear to be 



FIG. 15. Transmembrane action potentials recorded from a 

 single fiber of the A-V node (upper trace) and another single 

 fiber in His bundle (lower trace). A: control; B to E: acetyl- 

 choline effect; F: after elimination of acetylcholine. [From 

 Cranefield et al. (33).] 



identical. The potential from the A-V node was 

 referred to by the former group as a "slow potential" 

 and by the latter as a nodal "hump." In unipolar 

 records it consists of a slowly changing potential 

 which is negative in the upper A-V node, positive- 

 negative in the mid-nodal region and positive in the 

 lower node. The potential is unique in its lack of a 

 rapid negative-going phase (except at the nodobundle 

 junction where it is terminated by the rapid negative- 

 going bundle potential (figs. 13, 14). This potential 

 occupies the period of about 20 msec between the 

 excitation of atrial fibers at the upstream nodal region 

 and the excitation of the common bundle. The results 

 of these two studies differ remarkedly from those 

 reported by Alanis and co-workers (3), who are not 

 specific concerning either the type of electrode used 

 or the number of animals studied. Indeed, since these 

 investigators, in contrast to Pruitt and Essex, and 

 Scher et al., used no histologic controls, there is no 

 assurance that the potentials they report originated in 

 the A-V node. 



In Pruitt and Essex' study vagal stimulation 

 increased the width and altered the form of the nodal 

 "hump." They believe that \agal stimulation acts 

 within the node itself. In the study by Scher and co- 

 workers rapid stimulation usually increased the in- 

 terval between the atrial potential and the potential 

 from the A-V node (fig. 14). The site of first degree 

 A-V nodal block under most conditions was at the 

 junction between atrial and nodal cells. At times, 

 however, the nodal potential also increased in 

 duration. The conclusions of Scher and co-workers 

 about the location of first degree A-V block agree 

 with those of Hoffman and co-workers (58) and 



