PULMONARY infarction has never been produced consistently in experimental animals, although numerous investigators have attempted it.1 Virchow, in 1856,1k observed that obstruction of branches of the pulmonary artery was not in itself sufficient to result in infarction. Karsner in 1912,1f using turnip seed emboli in dogs, concluded that some factor other than an embolus was necessary to cause infarctions. Most authors reported that obstruction of branches of the pulmonary artery is not sufficient to cause infarction, if infarction is defined as necrosis of pulmonary tissue.
An exception is the work of Steinberg and Mundy,1i who produced occasional infarcts with employment of lead shot alone as emboli to occlude branches of the pulmonary artery. They, therefore, concluded that no factor except embolism is necessary to produce infarction.
Clinical observation long ago revealed that pulmonary infarction following an embolus occurred usually in patients who had concomitant pulmonary
CHAPMAN DW, GUGLE LJ, WHEELER PW. EXPERIMENTAL PULMONARY INFARCTION: Abnormal Pulmonary Circulation as a Prerequisite for Pulmonary Infarction Following an Embolus. Arch Intern Med (Chic). 1949;83(2):158–163. doi:10.1001/archinte.1949.00220310041004
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