Journal Article Bacterial Flora of the Lower Respiratory System of Normal Dogs Get access H. Livingstone, H. Livingstone Chicago Search for other works by this author on: Oxford Academic PubMed Google Scholar W. E. Adams W. E. Adams Chicago Search for other works by this author on: Oxford Academic PubMed Google Scholar The Journal of Infectious Diseases, Volume 48, Issue 3, March 1931, Pages 282–291, https://doi.org/10.1093/infdis/48.3.282 Published: 01 March 1931 Article history Received: 22 August 1930 Published: 01 March 1931
The relationship between massive atelectasis and pulmonary suppuration has been a subject of much controversy during the past few years. Some believe that once massive atelectasis has developed, a suppurative process is inevitable. Others, however, are of the opinion that a suppurative lesion develops only when the obstruction producing the atelectasis contains infective organisms; or when an embolus is engrafted upon an atelectatic area. The following experimental investigation was carried out to determine the effect of septic and aseptic emboli engrafted upon an atelectatic lung. Massive atelectasis of the left lung was produced in each of 8 dogs by the silver nitrate cauterization technique. Three emboli were introduced into the jugular vein of each animal, and subsequently lodged in the lung. Two of the emboli were infected with staphylococci, spirochetes, and fusiform bacilli; the third was sterile. Each emboli contained a lead pellet and could thus be located by roentgenogram. Results.—None of the animals died. They were sacrificed at the end of 11 days, 3 1/2 weeks, 5 weeks, 8 weeks, and 5 months. Gross, microscopic and roentgenologic examinations were made. Over 66 2/3% of the emboli lodged in the atelectatic
In a recent publication 1 on the subject of obstructive pulmonary atelectasis, two etiologic factors were described as being essential to its production, viz., bronchial obstruction and labored respiration or expiration against resistance. The latter of these two factors was contrary to the observations of Lee, 2 Coryllos and Birnbaum 3 and others, 4 who had produced the condition experimentally with regularity, and who believed a quiet, shallow respiratory cycle to be one of the important factors in its etiology. This idea has been carried down from the time of Pasteur 5 who, observing several cases of massive atelectasis associated with postdiphtheritic paralysis of the diaphragm, believed it due to a reduction in the depth of respiration. When an attempt was made to reproduce the results of other investigators, the factor of straining respiration was accidently encountered and massive atelectasis produced with routine regularity in its presence. That straining respiration
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