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1 From the Cardiovascular Department, Medical Research Institute, Michael Reese Hospital, Chicago, Illinois
The effect was studied of a number of drugs upon the severe bilateral pulmonary edema resulting from unilobar embolization of the lung, with 1 gm of starch. The edema in the embolized and nonembolized portions of the lung do not exhibit a uniform response to the several drugs tested. Intravenous Chlor-Trimeton, dibenamine, and Benodaine markedly inhibit its formation in the latter, but do not affect its appearance in the former. Procaine inhibits edema formation throughout the lungs. Its effect, however, is less marked in the injected than in the uninjected lobes. Atropine has an equivocal effect on the distant edema and no effect on that in the embolized lobe. The difference in response to drugs between the injected and the uninjected lung lobes suggests a possible difference in pathogenesis of the edema formation in these areas. The protective action of procaine on edema formation in the injected lobe suggests that a neural element may be involved acting on capillary permeability. In view of the ineffectiveness of antiadrenergic and antiparasympatholytic agents on the edema in this area, the possibility of axone-type reflex is suggested. However, the refractoriness of the local edema to the several drugs which exert a profound effect on the distant edema could also be due to an acute deterioration of capillary integrity accompanying the local trauma of massive embolization. The failure of Chlor-Trimeton to noticeably inhibit edema formation in the embolized lobe militates against histamine's importance in the genesis of the changes there. The marked inhibition of the edema formation in the nonembolized lung lends credence to the view that it is of the neurogenic or neuro-humoral variety.
Note:
in collaboration with Paul W. Saltzman, Carmen Rivera-Estrada and H. Gold
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