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RALPH D. CRESSMAN, M.D.; EDMUND W. BENZ, A.B.

Arch Surg. 1939;39(5):720-727.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

The role of the nervous system in the production of shock in the experimental animal has been emphasized by Slome and O'Shaughnessy,¹ who stated:^la "The initial depressor effect of trauma is due to fluid loss; the significant secondary decline to shock is caused by the continued and continuous discharge of nervous impulses from the traumatized area. The nervous factor operating alone can cause death." These experiments have been discussed by Blalock and Cressman.²

Direct evidence for a nervous factor was adduced by O'Shaughnessy and Slome^1a,c by comparing records of the action currents in the nerves to a traumatized limb before and after trauma with those of the action currents in the nerves to the untraumatized control limb of the same animal. They stated:^1a

No abnormal impulses are recognizable for three quarters of an hour to one hour after trauma; after this time an almost continuous . . . [Full Text PDF of this Article]

Author Affiliations
NASHVILLE, TENN.

From the Departments of Surgery and Physiology, Vanderbilt University.

Footnotes
Aided by a grant from the Division of Medical Sciences of the Rockefeller Foundation.

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