THE weed‐killer Paraquat (1,1′‐dimethyl‐4,4′‐dipyridyliurn dichloride, Gramoxone, ICI) is toxic not only to plants but also to animals including man. The predominant lesions induced by paraquat are found in the lungs and consist of collapse, hyaline membranes, haemorrhage, interstitial inflammation and proliferation of bronchiolar epithelium (Bullivant, 1966; Clark, McElligott and Hurst, 1966; Almog and Tal, 1967; Manktelow, 1967; Campbell, 1968; Matthew et al., 1968; Oreopoulos et al., 1968; Conning, Fletcher and Swan, 1969). The pathogenesis of these changes, which persist several days after the excretion of injected paraquat (Daniel and Cage, 1966), is obscure. However, the similarity between the pulmonary lesions in paraquat poisoning and those of newborn infants dying from idiopathic respiratory distress suggests some common pathogenic mechanism, possibly a derangement of surfactant (Manktelow).
The purpose of the present study is to analyse, by quantitative methods, the effect of paraquat on the surfactant system of the rat lung. In particular, we tried to find out whether experimental paraquat poisoning could be adopted as a model for the study of the idiopathic respiratory distress syndrome.