摘要
目的:探讨封闭群SD→SD大鼠心脏移植能否建立移植物慢性失功(chronic graft failureCGF)模型,缺血再灌注损伤(ischemia reperfusion injuryI/R)是否可加速CGF的进程。方法:采用雌性封闭群SD大鼠60只,分两组,对照组供心取下后立即进行心脏移植,冷缺血组供心取下后,先在4℃生理盐水中冷保存3h,然后再进行心脏移植。对照组于术后4、12、24w,缺血组于术后4、8、12w,取移植心脏分别行H E染色和M asson三色染色观察移植心的组织病理学改变。结果:移植后4w,冷缺血组与对照组相比较,心脏血管内膜增生评分均较低,两者无显著性差异,(1.6±0.48 vs1.2±0.32,P>0.05);移植后12w,两者心脏血管内膜增生评分有显著性差异(3.6±0.48 vs2.4±0.48,P<0.05),而且冷缺血组已发展为中度至重度血管病变;冷缺血组12w与对照组24w移植心血管内膜增生评分相比较,二者无统计学差异(3.6±0.48 vs4.0±0.40,P>0.05)。结论:采用封闭群SD→SD大鼠异位心脏移植来建立移植心CGF模型是可行的,I/R损伤可加快移植心CGF的进程,大大缩短了建模时间。
Objective： To investigate whether the heart transplantation between closed colony SD rats can establish a cardiac chronic graft failure model, and whether the ischemia reperfusion injury can accelerate this process. Method： 60 female closed colony of SD rats were divided into two group at random, control group and ischemia group. In control group, donor hearts were implanted into recipients immediately, however, in ischemia group, donor hearts were stored for 3 hrs at 4℃ in isotonic saline to induce an ischemic injury before transplantation. In control group, grafts were excised at 4, 12, and 24 weeks after transplantation, while in ischemia group, grafts were excised at 4, 8, and 12 weeks after transplantation. Graft vasculopathy and interstitial fibrosis were graded for degree of intimal thickening and myocardiac interstitial fibrosis using HE and Masson staining. Results： By the 4th week after transplantation, the graft vasculopathy in two groups showed no significant difference （ 1.6 ± 0.48 vs 1.2 ± 0.32 ,P〉0.05 ）, however, by the 12th week, there was a significant difference （ 3.6 ± 0.48 vs 2.4 ±0.48, P〈0.05 ） in the graft vasculopathy in two groups. By the 24th week, grafts in control group showed the characteristic of chronic graft failure, including graft vasculopathy, interstitial fibrosis, and inflammatory cells infilatration, however, grafts in ischemia group displayed similar leisons by the 12th week. There was no significant difference （ 3.6 ± 0.48 vs 4.0 ± 0.40,P〉0.05 ） in the graft vasculopathy between two groups. Conclusion： It is practicable to establish a cardiac chronic graft failure model between closed colony SD rats, and ischemia reperfusion injury, as an alloantigen independent factor, would accelerate the development of rat cardiac chronic graft vascular disease, which can save the time for establishing models.
出处
《重庆医科大学学报》
CAS
CSCD
2006年第1期58-62,共5页
Journal of Chongqing Medical University
