290 THE CIRCULATION OP THE BLOOD 



peated stimulation of large afferent nerves. Since the experiments are 

 usually performed on anesthetized animals, the effect of the anesthetic 

 has to be discounted in experimental work on the causes of shock. 



The first step in such an investigation is naturally to classify the 

 symptoms into primary and secondary, for on the success of the classi- 

 fication must depend the outcome of further investigation into the 

 problem. 



The earlier investigators were naturally attracted to the pronounced 

 fall in Uood pressure as the primary cause of shock. It is true that a 

 pronounced lowering will ultimately produce symptoms that are not 

 unlike those of shock, but on the other hand it can readily be shown that 

 this is a result only a symptom and not a cause of the condition. It 

 was believed by Crile that the fall in blood pressure depended on a 

 universal dilatation of the blood vessels caused by exhaustion of the tone 

 of the vasoconstrictor center. It has been clearly shown, however, that 

 the tone of this center is practically normal in shock, and that the arte- 

 rioles are maintained not in a dilated but in a contracted state, indicat- 

 ing clearly therefore that the low blood pressure must be dependent 

 upon inadequate output of blood from the heart. The evidence for this 

 conclusion is as follows: (1) W. T. Porter 26 and his collaborators have 

 shown that both pressor and depressor reflexes are perfectly normal 

 in a rabbit that is in a condition of extreme shock. It is particularly im- 

 portant that depressor effects were still obtained, since this indicates 

 that tonic activity of the center must still have been .present. (2) The 

 blood vessels in a shocked animal are in a contracted state. On opening 

 a vessel and observing the outflow of blood, an increase occurs when the 

 nerve to the blood vessel is cut. (3) This same fact has been shown by 

 Seelig and Joseph, 27 who cut the vasomotor nerve proceeding to the 

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

 dilatation of the vessels. Intense shock was then produced in the animal 

 in the usual way, 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, the lack of pronounced fall in blood pressure indicating that there 

 must be a compensatory constriction of the arterioles. Lastly (5), it 

 has been found by Morrison and Hooker 29 that the outflow of blood 

 from the perfused organs of a shocked animal is less than that from the 



