Jandík J, Endrys J, Rehulová E, Mráz J, Sedlácek J, De Geest H
University Hospital Gasthuisberg, Leuven, Belgium.
Cardiovasc Res. 1993 Jun;27(6):1076-83. doi: 10.1093/cvr/27.6.1076.
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.
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.
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.
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.
本研究旨在探讨:(1)慢性肺栓塞导致的支气管肺侧支循环是否能在肺静脉流出道受损后预防肺梗死的进展;(2)肺静脉流出道受损的情况下,肺急性栓塞后支气管肺侧支循环是如何形成的。
对52只杂种犬进行研究。36只为实验动物,16只为对照组。在两组实验犬中,通过结扎左肺静脉诱导单侧肺静脉流出道受损:(1)在双侧肺动脉栓塞前3个月;(2)在双侧肺动脉栓塞前1小时。在结扎后12天处死所有动物。通过血管造影评估支气管动脉的大小。在组织学检查时测量动脉的直径和壁厚。
在所有实验犬中,无论在肺静脉结扎前支气管动脉是否扩张,或肺静脉结扎后侧支循环是否开始形成,左肺栓塞远端均出现出血性梗死。肺静脉结扎是肺梗死发生的必要因素,因为肺静脉流出道完整的右肺栓塞区域未发生梗死。单纯肺静脉结扎不会导致支气管动脉扩张或肥大。肺动脉栓塞后,肺静脉流出道先前受损的左肺和肺静脉完整的右肺,支气管动脉均出现同样程度的增粗和肥大。
扩张的支气管肺循环不能预防肺静脉流出道受损的肺栓塞区域梗死的发生。支气管肺侧支循环的形成不受先前肺静脉流出道受损的影响。