Jandik J, Rehulová E, Endrys J, De Geest H
Department of Cardiology, University Hospital Gasthuisberg, Leuven, Belgium.
Cardiovasc Res. 1990 Jun;24(6):485-92. doi: 10.1093/cvr/24.6.485.
The aim was to study the fate of enlarged bronchial arteries after resolution of experimental pulmonary embolism.
Embolisation of the pulmonary arteries of both lungs was performed with intravenous gelfoam. Pulmonary pressure and pulmonary arteriolar resistance were measured 1 h, 40 d and 80 d after embolisation. Pulmonary angiography and aortography were performed at the same time to evaluate the pulmonary emboli and the collateral bronchopulmonary circulation. Aortography and gross pathological and histological examination of the lungs was performed after 80 d.
15 adult mongrel dogs of either sex were studied, weight 22-25 kg. Nine dogs were embolised and there were six controls.
All animals survived until 80 d. There was a rise (p less than 0.001) in mean pulmonary artery pressure and arteriolar resistance 1 h after embolisation. Pulmonary artery pressures and resistances were still raised 40 d after embolisation but had returned to normal after 80 d. Pulmonary arteriography at 1 h confirmed massive thromboembolism. After 40 d antegrade pulmonary blood flow was almost completely restored, and the thromboemboli had largely disappeared. Pulmonary angiograms were completely normal after 80 d. Aortography after 40 d showed a well developed collateral bronchopulmonary circulation, most pronounced in the lower lobes, which persisted unchanged until 80 d. Aortography and gross pathological and histological examination at necropsy confirmed the presence of hypertrophic well developed bronchial arteries to both lower lobes and to a lesser extent to the middle and upper lobes, with only a few organised and recanalised thrombi in segmental arteries of both lower lobes.
Our data show a temporal dissociation between the resolution of pulmonary thromboemboli in the present model and the eventual regression of developed bronchopulmonary collateral vessels. The mechanism of this dissociation could not be elucidated.
旨在研究实验性肺栓塞消退后增粗的支气管动脉的转归。
经静脉注入明胶海绵栓塞双侧肺动脉。栓塞后1小时、40天和80天测量肺动脉压力和肺小动脉阻力。同时进行肺血管造影和主动脉造影以评估肺栓塞及支气管肺侧支循环。80天后进行主动脉造影以及肺的大体病理和组织学检查。
对15只体重22 - 25千克的成年杂种犬（雌雄不限）进行研究。9只犬接受栓塞，6只为对照。
所有动物均存活至80天。栓塞后1小时平均肺动脉压力和小动脉阻力升高（p < 0.001）。栓塞后40天肺动脉压力和阻力仍升高，但80天后恢复正常。1小时时的肺血管造影证实存在大量血栓栓塞。40天后顺行性肺血流几乎完全恢复，血栓栓塞大部分消失。80天后肺血管造影完全正常。40天后的主动脉造影显示支气管肺侧支循环发育良好，在下叶最为明显，直至80天保持不变。尸检时的主动脉造影以及大体病理和组织学检查证实下叶存在肥厚且发育良好的支气管动脉，中叶和上叶程度较轻，下叶段动脉中仅有少量机化和再通的血栓。
我们的数据表明，在本模型中肺血栓栓塞的消退与已形成的支气管肺侧支血管最终消退之间存在时间上的分离。这种分离的机制尚无法阐明。
