Dodge-Khatami A, Backer C L, Holinger L D, Mavroudis C, Cook K E, Crawford S E
Northwestern University Medical School, Department of Surgery, Division of Cardiovascular-Thoracic Surgery, Children's Memorial Hospital, Chicago, Ill 60614-3394, USA.
J Thorac Cardiovasc Surg. 2001 Sep;122(3):554-61. doi: 10.1067/mtc.2001.116206.
In 1996, we introduced the free tracheal autograft technique for repair of congenital tracheal stenosis from complete tracheal rings in infants and children. Sources of possible concern with this procedure include the potential for autograft ischemia, patch dehiscence, and recurrent stenosis. Vascular endothelial growth factor is a potent angiogenic inducer (particularly in the setting of ischemia, hypoxia, or both) and is postulated to promote tissue healing. The purpose of this study was to test the hypothesis that pretreatment of tracheal autografts with topical vascular endothelial growth factor would enhance tracheal healing.
In a rabbit model of tracheal reconstruction (n = 32), an elliptically shaped portion of the anterior tracheal wall was excised. The excised portion of trachea was one third of the tracheal circumference and 2 cm in length (6 tracheal rings). This portion of trachea (the autograft) was soaked in either vascular endothelial growth factor (5 microg/mL, n = 16) or normal saline solution (n = 16) for 15 minutes before being reimplanted in the resultant tracheal opening. Animals were killed and autografts were examined at 2 weeks, 1 month, and 2 months postoperatively for gross and microscopic characteristics.
By 2 weeks, and progressing through 1 and 2 months, autografts treated with vascular endothelial growth factor, as compared with control autografts, had reduced luminal stenosis, submucosal fibrosis, and inflammatory infiltrate (P <.05). The autografts tended to become malaligned in control animals, whereas the tracheal architecture was preserved in rabbits treated with vascular endothelial growth factor. Microvascular vessel density was significantly greater in all vascular endothelial growth factor groups (P <.05) at all time intervals.
Topical treatment of free tracheal autografts with vascular endothelial growth factor in a rabbit tracheal reconstruction model enhanced healing, as evidenced by accelerated autograft revascularization, reduced submucosal fibrosis and inflammation, and preservation of the normal tracheal architecture. Topical vascular endothelial growth factor may improve future results of tracheal reconstruction.
1996年，我们引入了游离气管自体移植技术，用于修复婴幼儿先天性气管狭窄（由完整气管环引起）。该手术可能存在的问题包括自体移植组织缺血、补片裂开以及再发性狭窄。血管内皮生长因子是一种强效血管生成诱导剂（特别是在缺血、缺氧或二者并存的情况下），据推测它能促进组织愈合。本研究的目的是检验以下假设：用局部血管内皮生长因子预处理气管自体移植组织可促进气管愈合。
在兔气管重建模型（n = 32）中，切除气管前壁椭圆形部分。切除的气管部分为气管周长的三分之一，长度为2 cm（6个气管环）。该气管部分（自体移植组织）在重新植入气管缺损处之前，先在血管内皮生长因子（5μg/mL，n = 16）或生理盐水（n = 16）中浸泡15分钟。术后2周、1个月和2个月处死动物，检查自体移植组织的大体和微观特征。
到2周时，并持续至1个月和2个月，与对照自体移植组织相比，用血管内皮生长因子处理的自体移植组织管腔狭窄、黏膜下纤维化和炎性浸润均减轻（P <.05）。对照动物的自体移植组织往往出现排列不齐，而用血管内皮生长因子处理的兔气管结构得以保留。在所有时间点，所有血管内皮生长因子组的微血管密度均显著更高（P <.05）。
在兔气管重建模型中，用血管内皮生长因子局部处理游离气管自体移植组织可促进愈合，表现为自体移植组织血管再生加速、黏膜下纤维化和炎症减轻以及正常气管结构得以保留。局部应用血管内皮生长因子可能改善未来气管重建的效果。
