Department of Medical Specialities, Faculty of Medicine, Networking Research Center on Bioengineering, Biomaterials and Nanomedicine, University of Alcalá, Alcalá de Henares, Madrid, Spain.
Surgery. 2010 Mar;147(3):378-91. doi: 10.1016/j.surg.2009.10.011. Epub 2009 Dec 11.
In a high proportion of patients, operatively lysed adhesions reform. Using a rabbit adhesiogenesis model, this study assessed the efficacy of adhesiolysis and examined how this relates to the tissue composition of adhesions at the time of lysis.
Polypropylene meshes (5 x 3.5 cm) were implanted on the parietal peritoneum of New Zealand white rabbits. Some animals were killed 3, 7, 14, and 90 days postimplantation to obtain adhesion tissue. Adhesion formation/reformation was monitored by sequential laparoscopy in other animals kept for 90 days and in a separate experimental group subjected to adhesiolysis at 3 days postimplantation. Immune and inflammatory response markers were determined by immunohistochemical, Western blotting, and real-time reverse transcriptase polymerase chain reaction procedures in adhesion tissue; areas occupied by adhesions were quantified in meshes.
In animals undergoing adhesiolysis, mesh areas covered by adhesions were significantly decreased at each follow-up time and affected areas became mesothelialized. Increased transforming growth factor (TGF)-beta1 expression was detected in adhesions at 3 days. Greatest TGF-beta1 and vascular endothelial growth factor (VEGF) protein expressions were observed at 7 days, whereas genetic overexpression was noted at 14 days. Active inflammatory cells peaked at the 7-day time point.
Adhesions formed at 3 days; at this critical time, an adhesiolysis was effective in preventing reformation of future adhesions. TGF-beta1 gene and protein expression were increased in 3-day adhesions with respect to the omentum. Levels of active TGF-beta1 and VEGF were increased at 7 days, along with the inflammatory response at this time point related to tissue remodeling, which led to stabilization of adhesions.
在很大比例的患者中,手术松解的粘连会重新形成。本研究通过兔粘连形成模型评估了粘连松解的效果,并研究了其与粘连松解时粘连组织组成的关系。
在新西兰白兔的壁层腹膜上植入聚丙烯网(5 x 3.5 cm)。一些动物在植入后 3、7、14 和 90 天被处死,以获得粘连组织。通过对另一些动物进行连续腹腔镜检查来监测粘连形成/再形成,这些动物被保留 90 天,在一个单独的实验组中,在植入后 3 天进行粘连松解。通过免疫组织化学、Western blot 和实时逆转录聚合酶链反应程序测定粘连组织中的免疫和炎症反应标志物;在网片中定量测量粘连占据的面积。
在接受粘连松解的动物中,每个随访时间的网片上粘连覆盖面积显著减少,受累面积被间皮化。在 3 天的粘连中检测到转化生长因子(TGF)-β1 表达增加。在 7 天观察到最大的 TGF-β1 和血管内皮生长因子(VEGF)蛋白表达,而在 14 天则观察到基因过表达。活性炎症细胞在 7 天时间点达到峰值。
粘连在 3 天形成;在这个关键时期,粘连松解术有效地防止了未来粘连的形成。与大网膜相比,3 天的粘连中 TGF-β1 基因和蛋白表达增加。在 7 天,活性 TGF-β1 和 VEGF 水平增加,同时伴随着此时点与组织重塑相关的炎症反应,这导致粘连的稳定。