BRONCHIAL ARTERIES IN EXPERIMENTAL PULMONARY INFARCTION - ANGIOGRAPHIC AND MORPHOMETRIC STUDY

Objectives: The aim was to investigate (1) whether collateral bronchop ulmonary circulation developing due to chronic pulmonary embolism coul d prevent the evolution of pulmonary infarction after induction of pul monary venous outflow impairment; and (2) how collateral bronchopulmon ary circulation developed after acute embolisation of the lung with im paired pulmonary venous outflow. Methods: Fifty two mongrel dogs were studied. Thirty six dogs were experimental animals and 16 were in a co ntrol group. Unilateral impairment of pulmonary venous outflow was ind uced by constriction of the left pulmonary veins in two groups of expe rimental dogs: (1) three months after and (2) one hour before bilatera l embolisation of the pulmonary artery. All animals were killed 12 day s after constriction. The size of the bronchial arteries was evaluated from angiograms. The diameter and the wall thickness of the arteries were measured during histology. Results: In all experimental dogs, hae morrhagic infarctions developed distally to emboli in the left lung re gardless of whether the bronchial arteries were dilated before inducti on of pulmonary venous constriction or whether collateral circulation started to develop after pulmonary venous constriction. Constriction o f the pulmonary veins was an essential factor for pulmonary infarction to develop as no infarction developed in the embolised regions of the right lungs with intact pulmonary venous outflow. Pulmonary venous co nstriction alone did not cause dilatation or hypertrophy of the bronch ial arteries. After pulmonary artery embolisation, the same enlargemen t and hypertrophy of the bronchial arteries occurred both in the left lung with previously impaired venous outflow and in the right lung wit h intact pulmonary veins. Conclusions: Expanded bronchopulmonary circu lation did not prevent the development of infarction in the embolised region of the lung with impaired pulmonary venous outflow. Development of collateral bronchopulmonary circulation was not influenced by prev iously impaired pulmonary venous outflow.