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全身性炎症伴脑激活增强导致术后肠梗阻更严重的延迟。

Systemic inflammation with enhanced brain activation contributes to more severe delay in postoperative ileus.

机构信息

Tytgat Institute for Liver and Intestinal Research, Academic Medical Center, Amsterdam, The Netherlands.

出版信息

Neurogastroenterol Motil. 2013 Aug;25(8):e540-9. doi: 10.1111/nmo.12157. Epub 2013 May 27.

DOI:10.1111/nmo.12157
PMID:23711101
Abstract

BACKGROUND

The severity of postoperative ileus (POI) has been reported to result from decreased contractility of the muscularis inversely related to the number of infiltrating leukocytes. However, we previously observed that the severity of POI is independent of the number of infiltrating leukocytes, indicating that different mechanisms must be involved. Here, we hypothesize that the degree of tissue damage in response to intestinal handling determines the upregulation of local cytokine production and correlates with the severity of POI.

METHODS

Intestinal transit, the inflammatory response, I-FABP (marker for tissue damage) levels and brain activation were determined after different intensities of intestinal handling.

KEY RESULTS

Intense handling induced a more pronounced ileus compared with gentle intestinal manipulation (IM). No difference in leukocytic infiltrates in the handled and non-handled parts of the gut was observed between the two intensities of intestinal handling. However, intense handling resulted in significantly more tissue damage and was accompanied by a systemic inflammation with increased plasma levels of pro-inflammatory cytokines. In addition, intense but not gentle handling triggered enhanced c-Fos expression in the nucleus of the solitary tract (NTS) and area postrema (AP). In patients, plasma levels of I-FABP and inflammatory cytokines were significantly higher after open compared with laparoscopic surgery, and were associated with more severe POI.

CONCLUSIONS & INFERENCES: Not the influx of leukocytes, rather the manipulation-induced damage and subsequent inflammatory response determine the severity of POI. The release of tissue damage mediators and pro-inflammatory cytokines into the systemic circulation most likely contribute to the impaired motility of non-manipulated intestine.

摘要

背景

术后肠麻痹(POI)的严重程度据报道与浸润白细胞的数量成反比,与肌层收缩力降低有关。然而,我们之前观察到 POI 的严重程度与浸润白细胞的数量无关,这表明必须涉及不同的机制。在这里,我们假设组织损伤的程度决定了局部细胞因子产生的上调,这与 POI 的严重程度相关。

方法

在不同强度的肠道处理后,确定肠道转运、炎症反应、I-FABP(组织损伤标志物)水平和大脑激活。

主要结果

与温和的肠道操作(IM)相比,强烈的肠道操作会引起更明显的肠麻痹。在两种肠道处理强度之间,在处理和未处理的肠道部分,白细胞浸润没有差异。然而,强烈的肠道操作会导致明显更多的组织损伤,并伴有全身炎症,导致促炎细胞因子的血浆水平升高。此外,强烈但不温和的肠道操作会导致孤束核(NTS)和最后区(AP)中的 c-Fos 表达增强。在患者中,与腹腔镜手术相比,开放性手术后血浆中 I-FABP 和炎性细胞因子水平明显升高,与更严重的 POI 相关。

结论

不是白细胞的涌入,而是操作引起的损伤和随后的炎症反应决定了 POI 的严重程度。组织损伤介质和促炎细胞因子释放到全身循环中,很可能导致未操作肠道的运动障碍。

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