J.Jpn. Surg. Soc.. 53(2): 57-63, 1952

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Original article

EXPERIMENTAL STUDY OF REFLEX SHOCK

A large number of investigations have been made concerning the traumatic shock, particulary the secondary shock, and it has been believed by many authors that the secondary shock was mainly of toxic origin. But with respect to the primary shock, only a few investigations has been reported.
Generally it is considered that the primary shock is induced through a neurogenic reflex, but the detailed and precise mechanism is still unknown.
This experimental study in rabbits was undertaken to reveal that the reflex shock, in which bradycardia and low blood pressure are characteristic, could be or could not be produced by means of various interventions upon peripheral nerves and abdominal autonomic nerves.
Conclusions are as follows,
(1) A reflex shock did not result from the crushing of muscles, peripheral nerves and testicles.
(2) It was not produced by the stimulation of autonomic afferent fibers in the abdominal cavity.
(3) It developed by the injection of iodine into the pleural cavity. In this state there were low blood pressure and bradycardia.
(4) It also developed during the operative manipulation of carotid artery for the purpose of measuring blood pressure. When death followed low blood pressure and prebradycardia were characteristic features and respiratory arrest preceded cardiac arrest. It is presumed to have arisen from the stimulation of Hering's and aortic nerves.
(5) The experimental results were obtained in rabbits, but it is unknowm whether the results in other animals are the same or not. However, the author believes that the results must be same in the majority of other animals.
(6) If a primary shock is a reflex shock, it must be caused by the inhibition of cardiac action through vagus nerve, being elicited by stimulation from regions of chest, neck and head. Thus a primary shock is of cardiac origin.
Characteristic signs are low blood pressure and bradycardia. In rabbits, a reflex shock of this kind can not be elicited by stimulation of extremities and abdominal cavity.
(7) On the contrary, a secondary shock is not a reflex shock. It is of vascular origin in the periphery. Clinical manifestations are low blood pressure and tachycardia.
(8) Shock induced by spinal anesthesia is a neurogenic, but not reflex shock. It is due to the vasodilatation of splanchnic area, analogous to the condition following the ligation of the portal vein. It is allied to a secondary shock and there are low blood pressure and tachycardia. (author's abstract)

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