Boybeyi, OzlemSoyer, TutkuAtasoy, PinarGunal, Yasemin DereAslan, Mustafa Kemal2020-06-252020-06-252015closedAccess0022-34681531-5037https://doi.org/10.1016/j.jpedsurg.2014.05.036https://hdl.handle.net/20.500.12587/6224Soyer, Tutku/0000-0003-1505-6042Purpose: 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.eninfo:eu-repo/semantics/closedAccessHypertrophic pyloric stenosisPyloric muscleEnteral hormonesL-NAMEProstaglandinArticle50340841210.1016/j.jpedsurg.2014.05.0362-s2.0-8492405474125746698Q1WOS:000350825200009Q2