Anti-inflammatory Effect of Obstructive

Detailed clinical observations by Hench (1933, 1934) established that hepatogenous jaundice ameliorated rheumatoid arthritis and fibrositis. Reports followed of remissions attending jaundice induced by the injection of bile salts and bilirubin (Thompson and Wyatt, 1938), by inoculation with infectious jaundice (Gardner, Stewart, and MacCallum, 1945), and by lactophenin (Hanssen, 1942), in addition to the many remissions attributed to cinchophen toxic hepatitis. In rats also, jaundice caused by the ligation of the bile duct inhibited an experimental arthritis produced by the injection of formalin (Selye, 1950) or of pleuropneumonia-like organisms (Snow and Hines, 1941). Selye's interpretation of jaundice and arthritis in terms of stress and inflammatory processes suggested that the antiinflammatory effect of jaundice might be mediated by a hypersecretion of adrenal glucocorticoids (Selye, 1950). Subsequently, Selye (1954) provided evidence that an increased secretion of glucocorticoids is not prerequisite to a reduction of inflammatory processes during jaundice. He found that jaundice enhanced the anti-inflammatory effect of cortisone in adrenalectomized rats, and interpreted this as being due to a glucocorticoid-sensitizing principle in jaundice. A possibility that jaundice inhibited the inactivation of glucocorticoids was investigated by Baker (1955), and liver slices from jaundiced and non-jaundiced rats were found to inactivate equal amounts of hydrocortisone. The present study was undertaken to obtain additional information about the role of adrenocortical hormones in inflammatory processes during obstructive jaundice. Indices of adrenocortical hormone activity and inflammatory processes were the weights, respectively, of the thymus and of the