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WILLIAM B. NEAL, Jr., M.D.; EDWARD R. WOODWARD, M.D.; ALLAN E. KARK, M.B., F.R.C.S. (Eng.); JOSE M. ZUBIRAN, M.D.; J. ANTONIO MONTALBETTI, M.D.

AMA Arch Surg. 1952;65(5):774-782.

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

SEVERE burns are often fatal in both man and the experimental animal, despite adequate replacement of blood volume and electrolytes, the use of oxygen and antibiotics, and supportive therapy, including feeding, sedation, and early skin grafting. The role of the adrenal gland in burn mortality has been speculated upon extensively. Since the work of Selye¹ it has been well known that after a stress situation the adrenal gland becomes depleted of cholesterol and ascorbic acid and subsequently, in a matter of a few hours, exhibits a marked hyperplasia, as if an augmented production of cortical hormones was an important protective mechanism. Indeed, it has been shown that adrenocortical extract and cortisone enable the adrenalectomized animal to withstand certain stresses, i. e., work,² cold,³ and typhoid vaccine.⁴ The intact animal, however, is not protected by cortisone against the stress of limb ligation or radiation (Ingle⁵ and . . . [Full Text PDF of this Article]

Author Affiliations
CHICAGO

From the Department of Surgery, University of Chicago, The School of Medicine.

Footnotes
The supplies of corticotropin used in this research were generously supplied by Dr. Lawrence L. Lachat of Armour and Company, Chicago.

This research has been aided by grants from the Otho S. A. Sprague Memorial Institute and from the Douglas Smith Foundation for Medical Research of The University of Chicago.

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