to the vessels of one ear of a white rabbit and thus caused a local paralytic 

 dilatation of the vessels. Intense shock was then induced, after which 

 the blood pressure in the anterior part of the animal was suddenly raised 

 by applying a clamp to the abdominal aorta just below the diaphragm. 

 This increased blood pressure caused the vessels of the denervated ear to 

 become engorged with blood, but not those of the opposite normal ear, 

 which retained their tone (Fig. 106). (4) The volume of blood expelled 

 by the ventricles has been shown by Henderson 28 to be distinctly diminished 

 in the early stages of shock, before there is a pronounced fall in blood 

 pressure indicating that there must be a compensatory constriction of the 

 arterioles. 



To the foregoing evidence of a constricted condition of the arterioles 

 in shock, may be added the less direct evidence furnished by the. pallor 

 of the shocked patient and the indications that 'the sympathetic nervous 

 system, instead of being paralyzed, is in an excited state, as shown by 

 the sweating and the dilated pupils. 



Furthermore, we know from the experiments of Pike, Guthrie and 

 Stewart 30 that the vasomotor center can withstand complete anemia with- 

 out losing its tone or reflex activity, better than any of the other cardinal 

 centers. 



Those who have maintained that a deficiency in the tone of the vaso- 

 constrictor and other nerve centers is responsible for shock have based 

 their evidence partly on histological examination of nerve cells of shocked 

 animals, it being assumed that the chromatolysis shown by these cells 

 indicates an exhausted condition. The assumption is, however, entirely 

 unwarranted, and no regard is given to the well-established fact that 

 similar histological changes may be produced by other conditions. It 

 is certainly safe to conclude that the changes in the nerve cells in shock 

 are the result and not the cause of this condition. It may be, as suggested 

 by Mott, 38 that toxic substances liberated from damaged tissues are in 

 part, at least, responsible for the chromatolysis. 



Since the fall in arterial blood pressure occurs with contracted ar- 

 terioles, it must be dependent on a diminished discharge of blood from 

 the heart. Interference with the heart action itself (independently of 

 the blood carried to this organ), or a deficiency in the filling of the ven- 

 tricles during diastole, are the possible causes for the diminished output. 

 The possibility that the heart action itself has been interfered with, as for 

 example, by paralysis of the vagus mechanism, causing a rapid beating 

 and consequent shortening of the filling (diastolic) period of the heart, 

 has been shown to be untenable by various experiments. Thus, when 

 the arterial blood pressure is artificially raised, either by epinephrine in- 

 jection or by cerebral compression, the heart promptly responds to the in- 



