Department of Surgery, Brigham and Women's Hospital and Harvard Medical School, 75 Francis Street, Boston, MA, 02115, USA,
Langenbecks Arch Surg. 2013 Oct;398(7):997-1000. doi: 10.1007/s00423-013-1084-3. Epub 2013 May 17.
We investigated the hypothesis that local tissue ischemia is responsible for suture-induced adhesion formation.
A total of 160 interrupted sutures were placed in the parietal peritoneum of 20 Wistar rats. The animals were randomized into an ischemia group, where the sutures were pulled tight and a non-ischemia group, where the sutures were tied as loose loops with air knots to avoid any local ischemia. The midline laparotomy was closed with a running suture. On postoperative day 10, adhesions to the sutures were counted.
There was no statistically significant difference in the number of adhesions forming to sutures with local ischemia (n = 66/80) versus sutures without local ischemia (n = 69/80).
We conclude that local tissue ischemia is not necessary for suture-induced adhesion formation and propose an additional mechanical mechanism to explain how suture knots can predispose to adhesiogenesis.
我们研究了局部组织缺血是导致缝线引起粘连形成的假设。
总共在 20 只 Wistar 大鼠的壁层腹膜上放置了 160 个间断缝线。将动物随机分为缺血组,缝线拉紧;非缺血组,缝线系成松结空气结,以避免任何局部缺血。用连续缝线关闭正中剖腹术。术后第 10 天,计数缝线处的粘连。
局部缺血缝线(n=80 中的 66 个)与无局部缺血缝线(n=80 中的 69 个)形成的粘连数量无统计学差异。
我们得出结论,局部组织缺血不是缝线引起粘连形成所必需的,并提出了另一种机械机制来解释缝线结如何导致粘连形成。