Search

Background: Development of the human fetal stomach starts at the 4th week of intrauterine life. The knowledge of histogenesis of the musculature of the stomach is important for understanding, diagnosis, and treatment of gastric adenomyoma, congenital anomalies like congenital hypertrophic pyloric stenosis, and abnormalities in the development of the enteric nervous system. The aim of this study was to find out the histogenesis of the submucosa (SM), muscularis mucosa (MM), and muscularis externa (ME) in the human fetal stomach. Methodology: Sixty-three freshly aborted fetuses which were free from any gross abnormality were collected from the obstetrics and gynecology department and studied for 2 years. The fetuses were dissected, the stomach was removed, and the tissue was processed for a histological study. Staining was done by hematoxylin and eosin, Masson's trichrome, and Van Gieson's stain. Slides were studied under Zeiss branded light microscope using ×10 and ×40 objectives. Results: MM was discontinuous initially and became well defined by 21 weeks in the fundus and body and by the 23rd week in the pyloric region. The density of collagen fibers increased gradually in SM and was seen in bundles from the 23rd week onward. The thickness of SM was more than ME till 22 weeks, and after 27 weeks, it was less than that of ME. In the fundus and body of the stomach, till 18 weeks, ME consisted of two layers, with the inner oblique layer being thicker than the circular layer. The circular layer thickened gradually, and the longitudinal layer appeared by the 25th week. In the pyloric region, initially, there was only a circular layer. The oblique and longitudinal muscle layers appeared at 17–18 weeks and 25th week, respectively. The thickness of the circular layer was found to be more than that of the body from the 21st week onward and became much thicker at around the 27th week. The histological feature of MM, ME, and SM of the stomach resembled an adult pattern by the 28th week of gestational age. Conclusion: The findings of the present study about the time of appearance and further development of MM and ME and the thickness and formation of SM of the human fetal stomach are quite comprehensive. These findings are expected to aid in the knowledge of histogenesis of the stomach in the human fetuses and help in the diagnosis and treatment of various congenital anomalies and clinical conditions involving gastric connective tissue and musculature.

Prostaglandin E 2 (PGE 2 ) actions on intestinal motility are complex due the differential expression of the PGE 2 receptors EP1-EP4. We sought to determine the actions of PGE 2 on electrical pacemaker and contractile activity of the circular and longitudinal muscle layers of the murine small intestine. Intracellular microelectrode and isometric force measurements were performed to examine the effects of PGE 2 receptor activation on circular and longitudinal muscle layers. In the two muscle layers PGE 2 produced differential responses. In the circular muscle layer PGE 2 caused dose-dependent membrane hyperpolarization and reduction in slow wave amplitude, accompanied by a decrease in the amplitude of phasic contractions. Membrane hyperpolarization and the reduction in slow wave amplitude and phasic contractions were insensitive to TTX and L-NNA, but inhibited by the K ATP channel antagonist, glibenclamide. The actions of PGE 2 on the circular muscle layer were mimicked by the selective EP 2 and EP 4 agonists ONO AE1-259 and ONO AE1-329, respectively. The actions of PGE 2 were partially inhibited by the EP4 antagonist ONO AE3-208. The EP 1 agonist ONO DI-004 produced little effect while the EP3 agonist ONO AE-248 caused dose-dependent membrane depolarization. In comparison, PGE 2 produced increased tone and phasic contractions in the longitudinal muscle layer that was mimicked by ONO DI-004 and ONO AE-248, while EP 2 and EP 4 agonists had little effect on contractile activity. These data suggest that differential expression of PGE 2 receptors on intestinal muscle layers can produce antagonistic actions on intestinal motility.