296 THE CIRCULATION OF THE BLOOD 



ent upon the low arterial blood pressure, although some authors have 

 suggested that the loss of sensation may be dependent upon an increased 

 resistance or block at the synapses of the receptor neurons (page 803). 

 This suggestion depends on the fact, demonstrated by Sherrington, that 

 repeated stimulation of the receptors of a reflex arc produces fatigue 

 of that particular reflex, and that this fatigue must be resident in the 

 synapsis and not in the motor neuron, since the same motor neuron 

 that participated in the fatigue can still be called into activity by afferent 

 stimuli transmitted to its nerve cell through other sensory pathways 

 (see page 825). It is thought that in shock the frequent afferent stimula- 

 tion produces synaptic fatigue and therefore dulls the sensory responses 

 of the animal. The researches of Mann above referred to, in which he 

 shows that shock may occur without any demonstrable afferent stimuli 

 in the brain stem, would seem, however, to negative the above hypothesis. 



The raised threshold of sensory stimulation is no doubt an effect of the 

 low blood pressure. It has been shown, for example, by E. L. Porter 36 

 that when the arterial blood pressure is maintained at a uniform level, 

 the threshold stimulus for spinal cord reflexes remains practically uni- 

 form, but becomes promptly increased when the arterial blood pressure 

 is made to fall. Why a lower blood pressure should have this effect is, 

 however, difficult to understand in the light of the researches of Stewart 

 and his coworkers, who, as remarked above, found that the cells of the 

 central nervous system may endure total anemia for many minutes and 

 still recover their physiologic condition. It may be, however, that the 

 low blood pressure affects the conductivity of the synapsis. 



The muscular weakness is probably also dependent on low blood 

 pressure, for it has been found in animals that, when the arterial blood 

 pressure is lowered to about 90 mm. Hg, the muscles contract much less 

 efficiently than ordinarily. The fall in body temperature is dependent 

 upon the muscular inefficiency. 



In conclusion, it should be pointed out that W. T. Porter, in the inves- 

 tigation of acute shock met with at the front, has found that, in many 

 cases at least, the circulatory disturbance is due to a condition of fat 

 embolism. The fat is derived from the marrow of long bones, such as 

 the femur, by injuries which smash the bones. Porter's observations 

 are at least very suggestive. 



CIRCULATION REFERENCES 



(Monographs) 



Wiggers, C. J. : The Circulation in Health and Disease, Philadelphia, 1915. 

 Mackenzie, J. : Diseases of the Heart, Oxford Medical Publishers, ed. 2, 1910. 

 Lewis, Thomas: * Mechanism of the Heart Beat, 1911, Shaw & Son, Fetter Lane, 

 London. 



