Abnormalities of neuropeptides and neural markers in the esophagus of fetal rats with adriamycin-induced esophageal atresia

被引:26
作者
Cheng, W
Bishop, AE
Spitz, L
Polak, JM
机构
[1] UNIV HONG KONG,DEPT SURG,DIV PAEDIAT SURG,HONG KONG,HONG KONG
[2] HAMMERSMITH HOSP,ROYAL POSTGRAD MED SCH,DEPT HISTOCHEM,LONDON W12 0HS,ENGLAND
[3] INST CHILD HLTH,PAEDIAT SURG UNIT,LONDON,ENGLAND
[4] GREAT ORMOND ST HOSP CHILDREN,DEPT SURG,LONDON WC1N 3JH,ENGLAND
关键词
esophageal atresia; gastroesophageal reflux; neuropeptides; adriamycin;
D O I
10.1016/S0022-3468(97)90552-2
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
Background/Purpose: To investigate the distribution of neural markers and neuropeptides in esophageal atresia (EA). Methods: A fetal rat model with Adriamycin-induced EA was used. The animals were divided into four groups: (1) control group, (2) saline-injected group, (3) Adriamycin administered but without the development of EA; and (4) Adriamycin-induced EA group. Specimens of the distal esophagus from each group were immunostained using antibodies to S100, protein gene product 9.5 (PGP), somatostatin, vasoactive intestine peptide (VIP), bombesin, galanin, substance P, neuropeptide Y (NPY), calcitonin gene-related product (CORP), met-encephalin, nitric oxide synthase, and tyrosine hydroxylase. Results: The total cross-sectional area of the distal atretic esophagus was significantly smaller than controls (P=.01), the submucosa being the component most affected (0.0465 v 0.0234 mm). Immunoreactivity for S100 and galanin were significantly elevated in the atresia group (0.0288 v 0.0079 and .001 v 0.000). In addition, there was also an increase in CGRP and Substance P in the atretic group. Conclusion: The elevated levels of S100 and galanin could explain the disordered motility observed in patients who had esophageal atresia. Copyright (C) 1997 by W.B. Saunders Company.
引用
收藏
页码:1420 / 1423
页数:4
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