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内镜下硬化术后贲门胃纤维化。控制实验性反流的机制?

Fibrosis of gastric cardia after endoscopic sclerosis. Mechanism for control of experimental reflux?

作者信息

Carvalho P J, Donahue P E, Miidla I, Davis P E, Shen Y J, Bombeck C T, Nyhus L M

机构信息

Department of Surgery, University of Illinois, Cook County Hospital, Chicago 60612.

出版信息

Am Surg. 1990 Mar;56(3):163-6.

PMID:2316937
Abstract

Endoscopic sclerosis of the gastric cardia (ESGC) prevents experimental gastroesophageal reflux (GER) without changes in lower esophageal sphincter (LES) pressure and length. This study was performed to define the histologic appearance of the esophagus and stomach one year after ESGC. Four dogs were studied one year after ESGC with morrhuate sodium; ESGC had been performed at six sites, 1-3 cm distal to the esophagogastric junction. All animals had stable weight and eating habits at sacrifice. Light microscopy of the cardia and LES included morphometry of wall thickness (mm) and assessment of fibrosis (- to ). The esophagus had minimal changes; the gastric cardia had focal fibrosis, maximal on the greater curve, without any change difference in wall thickness. ESGC results in fibrosis of the gastric cardia, without significant changes in the esophagus. These changes prevent GER, possibly by preventing the initiation of a reflux event.

摘要

贲门内镜下硬化术(ESGC)可预防实验性胃食管反流(GER),而不改变食管下括约肌(LES)压力和长度。本研究旨在明确ESGC术后一年食管和胃的组织学表现。对4只接受过鱼肝油酸钠ESGC治疗一年的犬进行研究;ESGC在食管胃交界处远端1 - 3厘米处的6个部位进行。所有动物在处死时体重和饮食习惯稳定。对贲门和LES进行光镜检查,包括测量壁厚(毫米)和评估纤维化程度(-至)。食管变化极小;胃贲门有局灶性纤维化,在大弯侧最明显,壁厚无任何差异变化。ESGC导致胃贲门纤维化,食管无明显变化。这些变化可能通过阻止反流事件的发生来预防GER。

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Fibrosis of gastric cardia after endoscopic sclerosis. Mechanism for control of experimental reflux?内镜下硬化术后贲门胃纤维化。控制实验性反流的机制?
Am Surg. 1990 Mar;56(3):163-6.
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2
Endoscopic ultrasonography verifies effect on endoscopic treatment of reflux in dogs and man.
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3
Endoscopic control of gastro-esophageal reflux: status report.
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