Abstract

Background: Hirschsprung’s disease and other gut malformations commonly present with obstructive features of gut in pediatric age group. Problem of obstruction persists even after resection and anastomosis operation. Aims and Objectives: This in vitro comparative study was performed to assess the gut contractility to chemical mediators such as Acetylcholine and Histamine between Hirschsprung’s disease and other gut malformations. Materials and Methods: The longitudinal muscle strips of Hirschsprung’s cases and other gut malformations (non-Hirschsprung’s cases) were placed in Dales organ bath containing Krebs-Ringer solution, continuously bobbled with 100% O2 at 28°C. Gut contractions were recorded using Power Lab 4/ST system and was analyzed using software CHART-5 for windows. Control contractions were recorded against initial tension of 0.5 g. Subsequently, agonist (acetylcholine, histamine)- induced contractions were recorded before and after appropriate antagonists (atropine, pheniramine). Before values of agonist-induced contractions of Hirschsprung and non-Hirschsprung’s cases were compared. Values of agonist- induced contractions obtained after pretreatment with antagonists were also compared between Hirschsprung and non- Hirschsprung’s cases.
Results: Acetylcholine enhanced contractions in non-Hirschsprung’s cases and it caused small increase in amplitude of contractions in Hirschsprung’s cases. Atropine pretreatment blocked acetylcholine-induced contractions significantly in non-Hirschsprung’s cases, whereas it failed to block in the Hirschsprung’s cases. Histamine augmented contractions in both Hirschsprung and non-Hirschsprung’s cases. H1 antagonist, pheniramine failed to block the contractility in both the cases. Conclusion: Findings of this study suggested that acetylcholine increased gut contractility significantly in non-Hirschsprung’s cases involving muscarinic-cholinergic pathways, whereas histamine increased gut contractility in both Hirschsprung’s disease and non-Hirschsprung’s cases and it is not mediated by H1 receptors.