Abstract
IN 1950, Jensen, Dragsted and Kiaer,1 in Denmark, prepared the diethylaminoethyl ester of penicillin G and noted that it produced high levels in lungs and sputum after parenteral injection. Subsequently, they 2 , 3 showed that the hydriodide of this ester acted as a repository penicillin and also produced higher levels of penicillin in the lungs than either procaine penicillin or aqueous penicillin G (sodium salt). Clinical results in 13 cases of chronic bronchopulmonary infections and in 25 cases of pneumonia were highly favorable, the effects being exerted on penicillin-sensitive organisms.4 These results were confirmed in Great Britain by Heathcote and Nassau5 and . . .
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