Investigation of the effects of enteral hormones on the pyloric muscle in newborn rats

Yükleniyor...
Küçük Resim

Tarih

2015

Dergi Başlığı

Dergi ISSN

Cilt Başlığı

Yayıncı

W B Saunders Co-Elsevier Inc

Erişim Hakkı

info:eu-repo/semantics/closedAccess

Özet

Purpose: To investigate the effects of enteral hormones on pyloric muscle in order to clarify the etiopathogenesis of hypertrophic pyloric stenosis (HPS). Methods: Forty-two newborn Wistar-Albino rats were included. No intervention was done in the control group (CG, n = 6). In the sham group (SG, n = 6) 1 ml saline (0.9% NaCl solution), in the Nw-nitro-L-arginine methyl ester hydrochloride (L-NAME) group (LNG, n = 6) 100 mg/kg/d L-NAME, in the somatostatin group (STG, n = 6) 7 mcg/kg/d ST, in the cholecystokinin group (CCKG, n = 6) 3 mcg/kg/d CCK, in the substance P group (SPG, n = 6) 5 ml/kg/d SP, and in the prostaglandin-E1 group (PGE1G, n = 6) a cumulative dose of 360 mcg/kg PGE1 was given intraperitoneally for 14 days. On the 21st day, histopathological examination and muscle thickness measurements were done. Results were evaluated statistically. Results: Total and circular pyloric muscle thicknesses were significantly increased in the LNG compared to the CG and SG (p < 0.05). Circular pyloric muscle thickness was not increased in the STG, CCKG and SPG compared to the CG and SG (p > 0.05). In the PGE1G, muscle thickness was significantly decreased in the pylorus and increased in the antrum compared to the CG and SG (p < 0.05). Conclusion: Nitric oxide synthase (NOS) inhibition with L-NAME seems to be a causative factor in HPS by increasing pyloric muscle thickness. PGE predominantly affects antral gastric muscle and has no profound effect on pyloric muscle. (C) 2015 Elsevier Inc. All rights reserved.

Açıklama

Soyer, Tutku/0000-0003-1505-6042

Anahtar Kelimeler

Hypertrophic pyloric stenosis, Pyloric muscle, Enteral hormones, L-NAME, Prostaglandin

Kaynak

Journal Of Pediatric Surgery

WoS Q Değeri

Q2

Scopus Q Değeri

Q1

Cilt

50

Sayı

3

Künye

closedAccess