1 98 THE CONTRA CTION OF CARD I A C MUSCLE. 



In 1845, when the brothers Weber discovered the inhibitory action of the 

 vagus nerve upon the heart, it was known that the heart was also supplied 

 with fibres from the sympathetic system, and E. Weber, 1 in Wagner's " Hand- 

 wb'rterbuch," considered that the two nerves which went to the heart, vagus, 

 and sympathetic, were of opposite function ; that the latter were motor nerves, 

 and the former inhibitory. He was unable to obtain any effect from stimu- 

 lation of the sympathetic fibres themselves, but evidently looked upon those 

 nerves as entering at the aortic end of the heart, while the vagus entered at 

 the venous end ; for he says that the sympathetic fibres in the frog are 

 too delicate to stimulate, but by direct stimulation of the aorta he was able 

 to obtain acceleration, which he imagined to indicate that sympathetic fibres 

 passed into the heart in this direction. Continuing this idea, he pointed out 

 the difference between direct stimulation of the bulbus and ventricle on the 

 one hand, and of the vena cava and auricle on the other. In the former case 

 he obtained acceleration and increased systolic contraction, in the latter case 

 standstill in diastole and weaker contractions. 



Such then was Weber's conception : the heart was supplied with two 

 nerves, which entered at opposite ends, and their stimulation was opposite in 

 effect both on rate of rhythm and force of contraction. Of these two nerves 

 he and his brother clearly demonstrated that the inhibitory fibres ran in the 

 vagus nerve, but were unable to demonstrate the course and existence of the 

 accelerator fibres either in warm or cold-blooded animals. 



Following upon the great discovery of the brothers Weber, physiologists 

 were engaged for many years upon a controversy as to the meaning of this 

 standstill, the majority agreeing with Weber, that the inhibition of the heart 

 is caused by the vagus in the same way as inhibition by nervous action in the 

 central nervous system ; that, in fact, Weber's discovery did not imply the 

 discovery of a new class of nerves which acted on the muscular tissue in 

 the opposite direction to motor nerves, but rather that a motor nerve centre, 

 in the shape of the ganglion cells, existed in the heart, of the same character 

 as the centres in the central nervous system, the action of which the vagus 

 was able to inhibit. The strongest opponent of this view was SchifF, 2 who 

 objected in toto to the conception of inhibition, and maintained that the 

 vagus was the motor nerve of the heart up to its termination in the 

 muscular tissue, that the beat of the heart depended upon the stimulation of 

 the terminal nerve fibres in the heart itself, and that the so-called inhibition 

 was due to over-stimulation, causing exhaustion of these motor nerve fibres. 

 Schiff laid especial stress on the fact that direct stimulation of the muscular 

 tissue of the ventricle caused a local diastole of that part of the heart, so 

 that it remained relaxed and distended when the rest of the ventricle was 

 contracting; also, this effect was removed by atropine, just like the corre- 

 sponding effect of vagus stimulation. In other words, Schiff argued that the 

 terminal fibres of the motor vagus nerve in the muscular tissue could be 

 directly exhausted by over-stimulation as well as indirectly by stimulation of 

 the vagus trunk, and that therefore this experiment was clear evidence that 

 the vagus did not act by inhibiting any central nervous apparatus in the 

 shape of ganglion cells. 



Schiff's view that the vagus was the motor nerve of the heart, which was 

 easily exhausted by over-stimulation, was largely based upon the fact that a 

 weak stimulation of the frog's vagus often produced acceleration when a strong 

 stimulation produced inhibition. This acceleration upon stimulation of the 

 frog's vagus was noticed by many observers, especially by Wundt and Schelske 3 

 in 1859, after strong curari poisoning, but it was not until 1870 that Schmiede- 



1 " Handworterbuch d. Physiol.," 1846 (3), Bd. ii. S. 42-48. 



2 Arch. f. physiol. Heilk., Stuttgart, 1849, Bd. viii. 



3 Pcrhandl. d. naturh.-med. Vcr. zu Heidelberg, 1859. 



