310 THE CIRCULATION OF THE BLOOD 



ondary effect, and it is doubtful whether it is the only cause for the 

 depressed C0 2 -carrying power of the blood. 



In one or two cases the muscles were crushed in unanesthetized cats, 

 with the result that shock did not invariably follow, but this does not 

 invalidate the observations on anesthetized animals ; it only shows that, 

 as in histamine poisoning, the anesthetic weakens the resistance. When 

 the normal animals were bled before the crushing operation, shock super- 

 vened with certainty. 



Taking the results as a whole, and comparing them with clinical ex- 

 perience a very strong case is made for the hypothesis that surgical shock 

 is essentially due to intoxication by materialls derived from damaged 

 tissue. Shock is particularly common after severe tissue damage; rough 

 handling of the wound greatly aggravates it, whereas rigid care to 

 render the wounded part immobile is a valuable safeguard ; the adminis- 

 tration of ordinary anesthesia, (ether) to a shock patient- is notoriously 

 dangerous, whereas rapid amputation under nitrous oxide often ushers 

 in a steady recovery. All these clinical facts conform admirably with 

 the experimental findings. The above conclusions are more or less con- 

 firmatory of those drawn several years ago by Turck, 55 to whom credit 

 is due for being the first to suggest the toxemic element as a causative 

 factor in shock. 



With regard to the diagnostic value of measurement of the blood vol- 

 ume, it has been shown by Erlanger, Gasser and Meek 40 ' 41 that con- 

 centration of the blood becomes evident before the shock symptoms are 

 pronounced. This concentration is no doubt a most important factor 

 in causing curtailment of the volume of circulating fluid, not only be- 

 cause of loss of plasma, but also because it causes the corpuscles to be- 

 come contiguous so that they have a tendency to jam in the capillaries 

 and so lead to a progressively increasing under-nutritioii of the tissues 

 and the production of more toxic material. 



Cause of Secondary Symptoms 



It remains to consider the cause of some of the secondary conditions 

 developing in shock namely, the disturbances in sensation and motion 

 and the fall in body temperature. All of these are undoubtedly depend- 

 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 854). 

 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 



