背景:目前对增生性瘢痕预防和治疗的策略是有限的。
目标:为了促进这些努力,根据先前用于诱导缺血的方法,首次在兔耳中建立了微创性肥厚性瘢痕模型。
方法:研究了6只新西兰大白兔(共12只)。首先,缺血是通过结扎颅骨动脉来实现的,颅静脉和中央动脉,在保留尾动脉的同时,尾静脉和中央静脉,分别。手术时引起的缺血的相对水平,基线和最大灌注,通过荧光辅助血管造影术进行评估,并证明缺血耳的灌注率较低。血管损伤后,在腹耳上创建2cm全厚度线性伤口,并且在高张力下用4-0尼龙缝合线闭合。对于每一只兔子,一只耳朵接受了缺血和缝合张力损伤的组合(n=6),而另一只耳朵是非缺血性的,仅受伤和缝合张力(n=6)。
结果:术后四周,缺血性耳朵出现瘢痕肥大(组织学瘢痕厚度:1.1±0.2mm对0.5±0.1mm,p<0.05)。
结论:此处,我们描述了一部小说,典型的微创兔耳增生性瘢痕形成模型,可以研究预防瘢痕的新药。
BACKGROUND: Current strategies for hypertrophic scar prevention and treatment are limited.
OBJECTIVE: To facilitate these efforts, a minimally invasive hypertrophic scar model was created in a rabbit ear for the first time based on previous methods used to induce ischemia.
METHODS: Six New Zealand white rabbits (12 ears total) were studied. First, ischemia was achieved by ligating the cranial artery, cranial vein and central artery, while preserving the caudal artery, caudal vein and central vein, respectively. The relative level of ischemia induced at time of surgery, both baseline and maximum perfusion, was assessed with a fluorescent light-assisted angiography and demonstrated lower rates of perfusion in the ischemic ears. Following vascular injury, a 2-cm full thickness linear wound was created on the ventral ear and closed with 4 - 0 Nylon sutures under high tension. For each rabbit, one ear received a combination of ischemia and wounding with suture tension (n = 6), while the other ear was non-ischemic with wounding and suture tension alone (n = 6).
RESULTS: Four weeks post-operatively, ischemic ears developed scar hypertrophy (histological scar thickness: 1.1 ± 0.2 mm versus 0.5 ± 0.1 mm, p < 0.05).
CONCLUSIONS: Herein, we describe a novel, prototypical minimally invasive rabbit ear model of hypertrophic scar formation that can allow investigation of new drugs for scar prevention.