Experimental study of the mechanism that smoking can cause aneurismal change in the aorta

在病因上，重度吸烟者比不吸烟者有更多的潜在的主动脉壁扩大的风险。因此，我们的目的是通过药物递送系统来分析吸烟引起的动脉瘤样改变的机制。我们的假设是香烟中的化学物质会导致血管壁的破坏。分别制备了含0.7、7、70 mg的聚氯乙烯薄膜50 mg。我们用6只小猎犬作为动物模型。在全身麻醉下，行左侧开胸手术。胸主动脉显露。将含有苯并苯的PLCL膜直接附着在主动脉壁上。1个月后处死动物，切除胸主动脉。肉眼可见主动脉壁与肺之间有紧密粘连。组织学结果显示血管壁(外膜、中膜和内膜)的基本结构保持不变。未见纤维组织变薄。中性粒细胞明显渗入管壁组织，可能是苯并(A)芘引起的严重炎症反应。我们反复证实了这一事实。从主动脉外表面暴露苯并[a]并不是生理性的。壁内血栓位于内膜。苯并[2]从内表面暴露可能会导致墙体破坏。吸烟与主动脉壁瘤样改变之间的关系还需要进一步的分析。

The heavy smokers have more potential risk of enlargement of aortic wall than non-smoker etiologically. Thus our purpose is to analyze the mechanism that smoking can cause aneurismal change in the aorta by using drug delivery system. Our hypothesis is that chemical agents from cigarette can cause wall destruction in the vessel wall. We prepared 50mg of the PLCL film containing benzopyrene (0.7, 7, 70mg, respectively). We used 6 beagles as animal models. Under general anesthesia, left lateral thoracotomy was done. The thoracic descending aorta was exposed. The PLCL film containing benzopyrene was attached to the aortic wall directly. After one month, the dogs were sacrificed and the thoracic descending aorta was excised. There was tight adhesion between the aortic wall and the lung macroscopically. The histological findings revealed that the fundamental construction of vessel wall (adventitia, media, and intima) was maintained. The thinning of fibrous tissue was not observed. Neutrophil infiltration to the wall tissue was markedly observed, thus severe inflammation may be caused by benzopyrene. We confirmed the fact repeatedly. The exposure of benzopyrene from outer surface of the aorta is not physiological. Intramural thrombus was located at intima. The exposure of benzopyrene from inner surface may cause wall destruction. Further analysis will be needed in the relationship between smoking and aneurysmal change of the aortic wall.