RESISTANCE to general systemic stress in mammals has been characterized by adrenal hyperfunction as manifested by adrenal hypertrophy, adrenal cholesterol and ascorbic acid depletion, general lymphatic tissue involution and associated blood element changes (Selye, 1950). It is generally accepted that these responses are mediated through increased hypophysial corticotropin output. Similarly, a variety of stress stimuli have been shown to induce adrenal hypertrophy and lymphatic involution in birds (Garren and Shaffner, 1956; Siegel, 1960; Siegel and Siegel, 1961). Chronic or prolonged doses of exogenous corticotropin (ACTH) induce increases in adrenal weight and involution of lymphatic tissue in birds (Bates et al., 1940; Jailer and Boas, 1950; Zarrow and Baldini, 1952; Garren and Hill, 1958). Garren et al. (1961) have also observed that route and vehicle of application may modify responses. However, possibly as a result of greater functional independence of avian cortical tissue from the anterior pituitary (Brown et al., 1958; …
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H.S. Siegel (1962) studied this question.
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