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The adult respiratory distress syndrome (ARDS) is a life threatening complication with a high mortality rate which occurs in patients in a variety of situations. The diverse aetiologies of the syndrome have led to difficulties in defining and diagnosing those patients suffering from ARDS.This thesis describes the induction of pulmonary damage in two animal species, using a number of stimuli in an attempt to mimic the histological damage seen at autopsy in patients who have died of the adult respiratory distress syndrome. The intravenous administration of oleic acid in both mouse and rabbit induced fat embolism and lung pathology similar to that seen in some ARDS patients. In the rabbit these histological changes have been correlated with physiological measurements made during the course of the damage. In the anaesthetised, spontaneously breathing rabbit gram-negative scepticaemia, a major precursor of ARDS in humans, was induced by the intravenous administration of live E.Coli bateria. Physiological measurements relevant to pulmonary gas exchange efficiency were made during the course of the infusion of bacteria and for several hours after. The lung damage induced by gram-negative sepsis in the rabbit has been compared to that induced by oleic acid emoblism, E. Coli endotoxin and phorbol myristate acetate. The role of the polymorphonuclear leucocyte in the pathogenesis of lung damage induced by several of the stimuli used in these experiments has been studied in both the mouse and the rabbit models described in this thesis.

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The involvement of the thyroid hormones and corticosterone in the response to stressors, the influence of these hormones on the immune system and their possible role in the stress-induced changes in immune function, were investigated. Food and/or water deprivation, food restriction, exposure to heat or cold, all influenced serum thyroid hormone concentrations. Changes in food intake probably influenced serum concentrations of T3 and kT4 by reducing extrathyroidal 5 and 5' monodeiodination of T4. The effects on thyroid hormone concentrations, of heat, and possibly also cold and deprivation of water, were in part mediated by food intake. Deprivation of food or water, food restriction and cold all cause increases in circulating corticosterone. Though corticosterone influenced thyroid function in unstressed birds, it did not mediate the effects of underfeeding on serum T3 and T4. Circulating corticosterone was not increased during heat exposure, though changes in other physiological variables indicated a severe stress. It is concluded that circulating corticosterone cannot be relied upon as the sole index of stress. Thyroid hormones did not markedly affect humoral immunity, whereas corticosterone suppressed antibody production, probably by reducing T-helper cell function. Both thyroid hormones and corticosterone influenced cell-mediated immunity as evinced by changes in lymphoblastogenic responses to PHA and Con A. Food restriction, heat exposure and social stress suppressed PHA and/or Con A responses. However, these effects were not accounted for by the observed changes in thyroid hormones or corticosterone. It is concluded that although the thyroid hormones and corticosterone can influence cell-mediated immunity in unstressed birds, they are not directly responsible for the immuno-suppression associated with food restriction, heat or social stress.

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