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局部组织缺血对于缝线诱导的粘连形成不是必需的。

Local tissue ischemia is not necessary for suture-induced adhesion formation.

机构信息

Department of Surgery, Brigham and Women's Hospital and Harvard Medical School, 75 Francis Street, Boston, MA, 02115, USA,

出版信息

Langenbecks Arch Surg. 2013 Oct;398(7):997-1000. doi: 10.1007/s00423-013-1084-3. Epub 2013 May 17.

Abstract

BACKGROUND

We investigated the hypothesis that local tissue ischemia is responsible for suture-induced adhesion formation.

METHODS

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.

RESULTS

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).

CONCLUSION

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.

摘要

背景

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。

方法

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。

结果

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。

结论

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。

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