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THE FACT that many features of the shock syndrome are not un-like those of adrenal cortical insufficiency has suggested to some in-vestigators (Swingle et al., 1933) the possibility that the development of shock following injury may be the result of the failure of the secretory activity of this organ. Certainly the gross hemorrhagic ap-pearance, together with the depletion of the stainable lipid of the gland, indicate that the adrenal undergoes intense stimulation during shock. Furthermore, loss of the adrenals renders the animal hyper-sensitive to injury, a defect which may be, in part at least, corrected by cortical hormone therapy. That lack of cortical hormone is, how-ever, a limiting factor in the survival of the intact animal in shock has not been definitely established. Swingle and Remington (1944) have reviewed the great deal of conflicting data on this subject and have come to the conclusion that there has been no clear demonstration that cortical extract can protect against the development of shock in. the intact animal.
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Sayers et al. (1945) studied this question.
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