INHIBITION AND CARDIAC VAGUS 97 



" drainage," at least by the deduction that a muscle " went 

 out of action " owing to the fact that it sent no afferent, 

 and received no answering efferent messages. Yet as I 

 believed that there was a definitely active process shown 

 in the diastole on normal physiological stimulation, it at 

 last seemed certain that muscle-lengthening was not at all 

 an inhibitory but an exciting process. It did not seem 

 legitimate to say that lengthening took place " naturally," 

 even if the word was interpreted as implying local processes 

 of communicated strains, and cessation of strains, acting 

 directly as kinds of primitive reflexes. What then is the 

 action of muscle when lengthening ? As there are de- 

 formations of the muscle cells in contraction, why should 

 there not be active deformation in its opposite ? Such 

 deformations must depend on physico-chemical factors 

 such as surface tension and osmosis. If a muscle cell 

 alters its shape when stimulated to contract, we can 

 imagine its molecules ranged in a column of two, 

 " forming fours," and closing up. In the opposite 

 process the column of two molecules will become a 

 column of single ones. Thus relaxation becomes a 

 positive lengthening process of active deformation. If 

 there are no special muscles of diastole in the heart acted 

 on directly by the vagus as a motor nerve, some such 

 process must account for the active diastole. It was 

 a long time after some of these considerations occurred 

 to me that a real explanation of cardiac negative pressure 

 seemed possible. 



We find it, however, stated authoritatively that 

 stimulation of the cardiac vagus is followed, not by the 

 mere throwing out of action of another muscle, but by 

 a slowing of the rate, a diminution of the energy, and a 

 slackening in the rate of conduction of the Bundle of His and 

 7 



