Ozlem Boybeyi1, Tutku Soyer2, Pınar Atasoy3, Yasemin Dere Gunal4, Mustafa Kemal Aslan4. 1. Kırıkkale University, Medical Faculty, Department of Pediatric Surgery, Kırıkkale, Turkey. Electronic address: ozlemboy80@yahoo.com. 2. Hacettepe University, Medical Faculty, Department of Pediatric Surgery, Ankara, Turkey. 3. Kırıkkale University, Medical Faculty, Department of Pathology, Kırıkkale, Turkey. 4. Kırıkkale University, Medical Faculty, Department of Pediatric Surgery, Kırıkkale, Turkey.
Abstract
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) 1ml saline (0.9% NaCl solution), in the Nw-nitro-l-arginine methyl ester hydrochloride (L-NAME) group (LNG, n=6) 100mg/kg/d L-NAME, in the somatostatin group (STG, n=6) 7mcg/kg/d ST, in the cholecystokinin group (CCKG, n=6) 3mcg/kg/d CCK, in the substance P group (SPG, n=6) 5ml/kg/d SP, and in the prostaglandin-E1 group (PGE1G, n=6) a cumulative dose of 360mcg/kg PGE1 was given intraperitoneally for 14days. 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.
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) 1ml saline (0.9% NaCl solution), in the Nw-nitro-l-arginine methyl ester hydrochloride (L-NAME) group (LNG, n=6) 100mg/kg/d L-NAME, in the somatostatin group (STG, n=6) 7mcg/kg/d ST, in the cholecystokinin group (CCKG, n=6) 3mcg/kg/d CCK, in the substance P group (SPG, n=6) 5ml/kg/d SP, and in the prostaglandin-E1 group (PGE1G, n=6) a cumulative dose of 360mcg/kg PGE1 was given intraperitoneally for 14days. 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.