摘要
目的观察血管成形术后，病变近端正常参考血管重构的发生以及与病变部位血管重构的关系，并观察了粒细胞-巨噬细胞集落刺激因子（GM—CSF）对血管重构的影响。方法健康新西兰大白兔28只随机分为GM-CSF组和单纯损伤组。GM—CSF组皮下注射GM—CSF10μg·kg^-1·d^-1，单纯损伤组皮下注射同等量生理盐水。7d后球囊扩张损伤髂动脉。分别于术前、术后4周耳缘静脉采血检测一氧化氮（NO）浓度；4周后提取损伤动脉标本，观察内膜增生情况并测定病理形态学参数。结果术后4周GM—CSF组NO浓度（98±10）μmol／L高于单纯损伤组（83±12）μmol／L。单纯损伤组球囊损伤处血管残余管腔面积（LA）小于GM—CSF组[（0．87±0．40）mm^2vs（1．34±0．52）mm^2，P〈0．05]，损伤处内膜＋中膜面积（I＋M）大于单纯损伤组[（2．62±0．48）mm^2 vs （2．26±0．43）mm^2，P〈0．05]，两组损伤处外弹力膜环绕面积（EELA）差异无统计学意义[（3．48±0．80）mm^2 vs（3．60±0．91）mm^2，P〉0．05]。单纯损伤组参考血管LA小于GM-CSF组[（1．60±0．48）mm^2。vs（1．99±0．54）mm^2，P〈0．05]，两组参考血管I＋M无明显差异，LA与I＋M之间不存在相关性，而参考血管EELA与LA及I＋M之间有明显的相关性（r=0．91，P〈0．001；r=0．685，P〈0．001）。两组参考血管LA、EELA与损伤处血管LA、EELA也明显相关（r=0．919，P〈0．001；r=0．909，P〈0．001）。结论血管重构不仅发生在病变血管，同时也发生在近端参考血管。GM-CSF可以促进受损内皮细胞修复，改善负性血管重构。
Objective To observe the correlation of the arterial remodeling at the reference site and the lesion site and the effect of granulocyte-macrophage colony-stimulating factor （GM-CSF） on arterial remodeling. Methods 28 healthy New Zealand White rabbits were randomized to 2 equal groups ： GM-CSF group receiving subcutaneous injection of GM-CSF （ 10 μg · kg^-1 · d^-1 ） for 7 days, and pure damage group given subcutaneous injection of equivalent normal saline foe 7 days. Seven days later the iliac arteries of all animals were damaged by balloon. The levels of nitrogen monoxide （NO） were detected before and 4 weeks after angioplasty. Histological sections of iliac from rabbits killed 4 weeks after angioplasty were analyzed. Lumen area （ LA）, external elastic lamina area （ EELA）, and intimal plus medial areas （ I ± M） were measured at the lesion（L） and reference（R） sites. Results The NO levels 4 weeks later of the GM-CSF group was 98 ± 10 p.mol/L, significantly higher than that of the pure damage group （83 ± 12 μmol/L, P 〈 0. 05）. Morphometrie analysis showed that the LA^L） of the pure damage group was （O. 87 ± 0. 40 ） mm^2, significantly smaller than that of the GM-CSF group [ （ 1.34 ± 0. 52 ） mm^2, P 〈 0. 05 ]. The I ± M（L） of the pure damage group was （2. 62 ± 0. 48 ） mm^2, significantly greater than that of the GM-CSF group [ （ 2. 26 ± 0. 43）mm2, P 〈0. 05]. There was no statistical significance in the EEL（L） between the 2 groups [ （3.48 ± 0. 80） mm2 versus （ 3.60 ± 0. 91 ） mm^2, P 〉 0.05 ]. Morphometrie analysis showed that the LA（R） of the pure damage group was （1. 60 ± 0. 48 ） mm^2, significantly smaller than that of the GM-CSF group [ （ 1.99 ± 0. 54）mm^2 ,P 〈0. 05] , whereas there was no statistical significance in the I ± M（R） between the 2 groups. In both groups, LA（R） was significantly correlated with LA（L） （r=0. 919, P 〈 0.001 ）; and EELA（R） was significantly correlated with EELA（L） （ r = 0. 909, P 〈 0. 001 ） and I ± M（R） （ r = 0. 685 ; P 〈 0. 001 ）. Conclusion Remodeling affects both the lesion and the reference sites and appears to occur in parallel and proportionately at both sites. GM-CSF treatment increases re-endothelialization of the injured artery and inhibits unfavorable remodeling.
出处
《中华医学杂志》
CAS
CSCD
北大核心
2008年第36期2566-2569,共4页
National Medical Journal of China
基金
山东省自然科学基金资助项目（Y2005C70）
山东省科技攻关计划资助项目（2007GG20002045）
