Sagatun Liv, Jianu Constantin S, Fossmark Reidar, Mårvik Ronald, Nordrum Ivar S, Waldum Helge L
Department of Gastroenterology and Hepatology, St Olavs Hospital , Trondheim , Norway.
Scand J Gastroenterol. 2014 Oct;49(10):1173-80. doi: 10.3109/00365521.2014.950979. Epub 2014 Aug 26.
Vagotomy causes inhibition of basal and post-prandial acid secretion in humans, but the knowledge about the trophic effect of the vagal nerves is limited. Vagotomy is known to induce hypergastrinemia and we aimed to study the long-term effects of proximal gastric vagotomy (PGV) on the oxyntic mucosa and the enterochromaffin-like (ECL) cell density in particular.
Eleven patients operated with PGV because of duodenal ulcer and age- and sex-matched controls were examined 26 to 29 years postoperatively by gastroscopy with biopsies from the antrum and oxyntic mucosa. Neuroendocrine cell volume densities were calculated after immunohistochemical labeling of gastrin, the general neuroendocrine cell marker chromogranin A (CgA) and the ECL cell marker vesicular monoamine transporter 2 (VMAT2). Gastritis was graded and Helicobacter pylori (H. pylori) status was determined by polymerase chain reaction of gastric biopsies. Fasting serum gastrin and CgA were measured.
Serum gastrin was higher in the PGV group compared to controls (median 21.0 [interquartile range (IQR) = 22.0] pmol/L vs 13.0 [IQR = 4.0] pmol/L, p = 0.04). However, there was neither a significant difference in serum CgA or in CgA (neuroendocrine) nor VMAT2 (ECL cell) immunoreactive cell volume density in the oxyntic mucosa. There was significantly more inflammation and atrophy in H. pylori-positive patients, but PGV did not influence the grade of gastritis.
Despite higher serum gastrin concentrations, patients operated with PGV did not have higher ECL cell mass or serum CgA. Vagotomy may prevent the development of ECL cell hyperplasia caused by a moderate hypergastrinemia.
迷走神经切断术可抑制人体基础和餐后胃酸分泌，但关于迷走神经营养作用的了解有限。已知迷走神经切断术会诱发高胃泌素血症，我们旨在特别研究近端胃迷走神经切断术（PGV）对胃体黏膜和肠嗜铬样（ECL）细胞密度的长期影响。
11例因十二指肠溃疡接受PGV手术的患者以及年龄和性别匹配的对照组在术后26至29年接受胃镜检查，并从胃窦和胃体黏膜取活检组织。在对胃泌素、一般神经内分泌细胞标志物嗜铬粒蛋白A（CgA）和ECL细胞标志物囊泡单胺转运体2（VMAT2）进行免疫组织化学标记后，计算神经内分泌细胞体积密度。对胃炎进行分级，并通过胃活检组织的聚合酶链反应确定幽门螺杆菌（H. pylori）感染状况。检测空腹血清胃泌素和CgA水平。
PGV组血清胃泌素水平高于对照组（中位数21.0 [四分位间距（IQR）= 22.0] pmol/L vs 13.0 [IQR = 4.0] pmol/L，p = 0.04）。然而，胃体黏膜中血清CgA、CgA（神经内分泌）免疫反应性细胞体积密度或VMAT2（ECL细胞）免疫反应性细胞体积密度均无显著差异。H. pylori阳性患者的炎症和萎缩明显更严重，但PGV并未影响胃炎分级。
尽管血清胃泌素浓度较高，但接受PGV手术的患者ECL细胞量或血清CgA并未升高。迷走神经切断术可能会阻止由中度高胃泌素血症引起的ECL细胞增生的发展。
