| Abstrakt: |
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 |
