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肠道缺血/再灌注损伤会加重滑石粉诱导的大鼠粘连。

Intestinal ischemia/reperfusion injury aggravates talc-induced adhesions in rats.

作者信息

Murata Pin, Kase Yoshio, Tokita Youhei, Takeda Shuuichi, Sasaki Hiroshi

机构信息

R&D Division, Tsumura & Co., 2 Rokubancho, Tokyo, Japan.

出版信息

J Surg Res. 2006 Sep;135(1):45-51. doi: 10.1016/j.jss.2006.03.002. Epub 2006 May 2.

Abstract

BACKGROUND

Postoperative intraperitoneal adhesions are the leading cause of intestinal obstruction, but the underlying mechanisms remain incompletely understood. The aim of the current study was to investigate the involvement of intestinal ischemia/reperfusion (I/R) injury in adhesion formation in rats.

MATERIALS AND METHODS

Rats were subjected to either a dusting of talc (15 mg/rat) over the entire small intestine or ischemia induced by clamping the superior mesenteric artery (SMA) for 30 min followed by reperfusion with or without talc dusting. On postoperative days 4, 7, and 14, the scores, lengths, and incidence of adhesions were evaluated. In addition, the contractile force of the jejunal muscle was measured at 0, 24, 48, and 96 h after the treatments using organ bath techniques under bethanechol-stimulated conditions.

RESULTS

Talc induced mild adhesions in rats. Although I/R injury alone did not produce adhesions, it markedly aggravated the talc-induced adhesions, with higher scores and longer adhesions on postoperative days 4, 7, and 14. In addition, I/R injury caused 75-88% suppression of the circular muscle contractile force and 35-52% suppression of the longitudinal muscle contractile force at 24 h after SMA occlusion. However, talc did not affect the contractions.

CONCLUSIONS

Intestinal I/R injury aggravated the talc-induced adhesions, and this consequence might be due to the functional suppression of jejunal muscle contractions. This finding suggests that intestinal ischemia is an important factor in the etiology of postoperative adhesions.

摘要

背景

术后腹腔粘连是肠梗阻的主要原因,但其潜在机制仍未完全明确。本研究旨在探讨肠缺血/再灌注(I/R)损伤在大鼠粘连形成中的作用。

材料与方法

对大鼠进行以下处理:在整个小肠上撒滑石粉(15毫克/只),或夹闭肠系膜上动脉(SMA)30分钟诱导缺血,随后再灌注,再灌注时有无滑石粉撒布。在术后第4、7和14天,评估粘连的评分、长度和发生率。此外,在处理后0、24、48和96小时,使用器官浴技术在氨甲酰甲胆碱刺激条件下测量空肠肌肉的收缩力。

结果

滑石粉在大鼠中诱导轻度粘连。虽然单独的I/R损伤未产生粘连,但它显著加重了滑石粉诱导的粘连,在术后第4、7和14天粘连评分更高且粘连更长。此外,在SMA闭塞后24小时,I/R损伤导致环行肌收缩力抑制75 - 88%,纵行肌收缩力抑制35 - 52%。然而,滑石粉不影响收缩。

结论

肠I/R损伤加重了滑石粉诱导的粘连,这种结果可能是由于空肠肌肉收缩功能受抑制。这一发现表明肠缺血是术后粘连病因中的一个重要因素。

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