Abstract

Background An association between hydrocephalus and gastroesophageal motor abnormalities that cause gastroesophageal reflux (GER) is well known. Our aim was to investigate hydrocephalus-induced alterations in esophageal and gastric smooth muscle reactivity and their modulation by pharmacological interventions in the rat model. Materials and methods Hydrocephalus was induced in infantile rats by injection of kaolin into the cisterna magna. Hydrocephalic and sham-operated rats were exsanguinated 2 weeks after surgery. Esophageal and gastric fundus smooth muscle strips were studied in vitro for their contractile and relaxant response to receptor activation in the organ chambers set up. Additionally, esophageal and gastric tissue specimens were examined histologically for GER-induced changes. Results No histological evidence of esophageal and gastric changes reflecting GER was observed in the specimens of the control and hydrocephalus-induced rats. Maximum contractile responses of esophageal and gastric fundus smooth muscle to KCl and muscarinic receptor agonist carbachol were increased in the hydrocephalic groups compared with the control groups. These changes were statistically significant. Relaxant responses to beta adrenoceptor agonist isoprenaline were similar in the esophageal muscle strips of both hydrocephalic groups and the control groups. However, isoprenaline-induced relaxant responses of the gastric fundus muscle strips in the hydrocephalus-induced groups were significantly decreased as compared with the control groups. The relaxant responses to papaverine in the esophageal and gastric fundus smooth muscle strips were similar in the two groups. Conclusions Our study revealed alterations of receptor-dependent and receptor-independent foregut smooth muscle reactivity in the hydrocephalus-induced rat pups. Therefore, we suggest that impaired smooth muscle reactivity at least in part may contribute to abnormalities of foregut motor function seen in patients with hydrocephalus.

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