Studies of experimental pulmonary embolism and infarction and the development of collateral circulation in the affected lung lobe.

Abstract

Abstract 1.1. It is possible to produce pulmonary infarction regularly by the use of foreign body emboli in dogs with peripheral arteriovenous fistulas. 2.2. Dogs with normal circulation infrequently develop infarction of the lungs following pulmonary embolism. It has been shown that the bronchial arterial circulation to the embolized lobe becomes greatly increased, possibly protecting the tissue following embolic obstruction. In "fistula dogs" which have sustained pulmonary infarction after embolization, the development of marked enlargement of the bronchial arterial system is entirely comparable. 3.3. The evidence suggests that the effects of the bronchial arterial collateral system are offset acutely in the presence of a functioning arteriovenous shunt in the systemic circulation, permitting partial necrosis and eventual fibrosis of the injured lung. However, the collateral circulation is sufficiently large to prevent gangrenous necrosis. 4.4. We could find no evidence that pulmonary arterial intercapillary anastomoses contributed significantly to the formation of a collateral blood supply in embolized lung parenchyma.