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

吸烟引起主动脉瘤改变机制的实验研究

• 批准号: 17591454
• 负责人: SAIKI Yoshikatsu
• 金额: $ 2.41万
• 依托单位: Tohoku University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2005
• 资助国家: 日本
• 起止时间: 2005 至 2007
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-17591454/
• 关键词: Smoking; Aortic aneurysm; Drug delivery system; ドラッグデリバリーシステム; ベンゾピレン; ニコチン

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.

从病因学上讲，重度吸烟者比非吸烟者有更大的主动脉壁扩大的潜在危险。因此，我们的目的是通过药物传递系统来分析吸烟引起主动脉血管病变的机制。我们的假设是香烟中的化学物质会导致血管壁的破坏。我们制备了50mg的含有苯并芘（分别为0.7、7、70mg）的PLCL膜。我们用6只比格犬作为动物模型。在全身麻醉下，进行左外侧开胸术。胸降主动脉暴露。将含有苯并芘的PLCL膜直接附着于主动脉壁。一个月后，处死犬，切除胸降主动脉。肉眼可见主动脉壁与肺之间紧密粘连。组织学结果显示，血管壁的基本结构（外膜、中膜和内膜）得以维持。未观察到纤维组织变薄。可见神经元浸润于管壁组织，可能是苯并芘引起的严重炎症。我们反复证实了这一事实。从主动脉外表面暴露苯并芘不是生理性的。壁内血栓位于内膜。苯并芘从内表面暴露可引起壁破坏。吸烟与主动脉壁病变的关系有待进一步分析。