Abstract：
Abdominal aortic aneurysm (AAA) is a vascular disease that involves aortic wall dilation. Cigarette smoking is an established risk factor and rupture, and nicotine may be a major contributor to the onset of AAA. In humans the condition is associated with stenosis of the vasa vasorum (VV), which may be caused by nicotine. In this study, we evaluated the effects of nicotine on VV pathology. After 4 weeks of nicotine administration to rats using an osmotic pump, the VV patency rate in the nicotine administration group was significantly lower than that in the control group. The levels of Ki-67, a cell proliferation marker, were significantly increased in the regions containing VV in the nicotine group, as were hypoxia inducible factor-α levels. Collagen levels around VV were significantly lower in the nicotine group than in the controls. Our data suggest that nicotine can cause VV stenosis by inducing abnormal proliferation of smooth muscle cells in the VV. The increased risk of AAA development due to cigarette smoking may be partially explained by nicotine-induced VV denaturation and collagen fiber degradation.
摘要：
腹主动脉瘤（AAA）是一种涉及主动脉壁扩张的血管疾病。吸烟是一个既定的危险因素和破裂，尼古丁可能是AAA发病的主要原因。在人类中，这种情况与血管狭窄（VV）有关，这可能是由尼古丁引起的。在这项研究中,我们评估了尼古丁对VV病理的影响。用渗透泵给大鼠服用尼古丁4周后，尼古丁给药组的VV通畅率明显低于对照组。细胞增殖标志物Ki-67的水平，在尼古丁组中含有VV的区域显着增加，缺氧诱导因子-α水平也是如此。尼古丁组VV周围的胶原蛋白水平显着低于对照组。我们的数据表明，尼古丁可以通过诱导VV中平滑肌细胞的异常增殖而导致VV狭窄。吸烟导致的AAA发展风险增加可能部分解释为尼古丁诱导的VV变性和胶原纤维降解。
