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大鼠迷走神经切断术所致急性胃黏膜损伤的机制

The mechanism of vagotomy-induced acute gastric mucosal injury in the rat.

作者信息

Salim A S

机构信息

University Department of Surgery, Royal Infirmary, Glasgow, United Kingdom.

出版信息

Am J Med Sci. 1989 Jun;297(6):343-7. doi: 10.1097/00000441-198906000-00002.

DOI:10.1097/00000441-198906000-00002
PMID:2735340
Abstract

The present study investigated the integrity of the rat gastric mucosa after 6 hours of vagotomy without drainage. Transection vagotomy was employed to ensure complete gastric vagal denervation. Vagotomy without drainage produced gastric distension and mucosal injury confined to the glandular part. Anterior truncal vagotomy produced injury in 70% of rats, whereas truncal or transection vagotomy produced injury in all rats. The injury score with transection vagotomy was significantly higher than that with anterior truncal (21.2 mm2 +/- 1.6 vs. 8 mm2 +/- 2.7, mean +/- SEM, n = 10, p less than .01) or truncal vagotomy (21.2 mm2 +/- 1.6 vs. 15.6 mm2 +/- 1.4, mean +/- SEM, n = 10, p less than .05). Histologic examination of the mucosal injury revealed necrosis involving the epithelium and lamina propria. Cholestyramine, pyloroplasty, or gastric diversion protected the stomach against the vagotomy-induced mucosal injury. The results demonstrate in the rat that vagotomy without drainage produces within 6 hours injury of the gastric mucosa, which increases as vagal denervation is rendered more complete. Because cholestyramine protects the rat stomach against vagotomy-induced acute gastric mucosal injury, reflux of duodenal contents appears to be the principal factor behind this injury. Pyloroplasty prevents gastric distension but probably not duodenal contents refluxing, suggesting that this distention also may have a role in the mechanism of the said injury.

摘要

本研究调查了无引流迷走神经切断术后6小时大鼠胃黏膜的完整性。采用横断迷走神经切断术以确保完全切断胃迷走神经。无引流迷走神经切断术导致胃扩张和仅局限于腺部的黏膜损伤。前干迷走神经切断术在70%的大鼠中造成损伤,而全干或横断迷走神经切断术在所有大鼠中均造成损伤。横断迷走神经切断术的损伤评分显著高于前干迷走神经切断术(21.2平方毫米±1.6 vs. 8平方毫米±2.7,均值±标准误,n = 10,p < 0.01)或全干迷走神经切断术(21.2平方毫米±1.6 vs. 15.6平方毫米±1.4,均值±标准误,n = 10,p < 0.05)。对黏膜损伤的组织学检查显示坏死累及上皮和固有层。消胆胺、幽门成形术或胃转流术可保护胃免受迷走神经切断术引起的黏膜损伤。结果表明,在大鼠中,无引流迷走神经切断术在6小时内可导致胃黏膜损伤,且随着迷走神经切断更彻底,损伤会加重。由于消胆胺可保护大鼠胃免受迷走神经切断术引起的急性胃黏膜损伤,十二指肠内容物反流似乎是这种损伤背后的主要因素。幽门成形术可防止胃扩张,但可能无法防止十二指肠内容物反流,这表明这种扩张在上述损伤机制中也可能起作用。

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