Bronchial arteries in experimental pulmonary infarction: angiographic and morphometric study.
OBJECTIVE
The aim was to investigate (1) whether collateral bronchopulmonary circulation developing due to chronic pulmonary embolism could prevent the evolution of pulmonary infarction after induction of pulmonary venous outflow impairment; and (2) how collateral bronchopulmonary circulation developed after acute embolisation of the lung with impaired pulmonary venous outflow.


METHODS
Fifty two mongrel dogs were studied. Thirty six dogs were experimental animals and 16 were in a control group. Unilateral impairment of pulmonary venous outflow was induced by constriction of the left pulmonary veins in two groups of experimental dogs: (1) three months after and (2) one hour before bilateral embolisation of the pulmonary artery. All animals were killed 12 days 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, haemorrhagic infarctions developed distally to emboli in the left lung regardless of whether the bronchial arteries were dilated before induction of pulmonary venous constriction or whether collateral circulation started to develop after pulmonary venous constriction. Constriction of 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 constriction alone did not cause dilatation or hypertrophy of the bronchial arteries. After pulmonary artery embolisation, the same enlargement and hypertrophy of the bronchial arteries occurred both in the left lung with previously impaired venous outflow and in the right lung with intact pulmonary veins.


CONCLUSIONS
Expanded bronchopulmonary circulation 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 previously impaired pulmonary venous outflow.
Jandík
J
J
University Hospital Gasthuisberg, Leuven, Belgium.
Endrys
J
J
Rehulová
E
E
Mráz
J
J
Sedlácek
J
J
De Geest
H
H
D000818:Animals; D001027:Aortography; D001794:Blood Pressure / Q000502:physiology; D001981:Bronchial Arteries / Q000000981:diagnostic imaging / Q000473:pathology*; D003097:Collateral Circulation / Q000502:physiology*; D004285:Dogs; D005260:Female; D008297:Male; D011651:Pulmonary Artery / Q000503:physiopathology; D011652:Pulmonary Circulation / Q000502:physiology; D011655:Pulmonary Embolism / Q000000981:diagnostic imaging / Q000473:pathology*