The effect of N-methyl-D-aspartate receptor antagonist (memantine) on esophageal and gastric smooth muscle: functional investigation in a rat hydrocephalus model.

OBJECT: The purpose of this study was to investigate the effect of N-methyl-d-aspartate (NMDA) receptor antagonist on esophageal and gastric smooth muscle reactivity in a rat hydrocephalus model.

MATERIAL AND

METHODS

Hydrocephalus was induced in rats by injection of kaolin into the cisterna magna. Two weeks after the procedure, memantine (20 mg/kg per day, 2 weeks) was given to rats with hydrocephalus in the memantine group (MG). The rest of the rats with hydrocephalus received serum physiologic (hydrocephalus group, HG). The control group (nonhydrocephalic rats, CG) was sham operated. The fourth group consisted of nonhydrocephalic rats with treated memantine (memantine control group, MC). Contractile (KCl, carbachol) and relaxant (isoprenaline, papaverine) esophageal and gastric smooth muscle reactivity were determined by in vitro muscle technique.

RESULTS

No significant difference was found in the KCl (nonreceptor-mediated)-induced esophageal smooth muscle reactivity among the groups. Carbachol (receptor-mediated)-induced smooth muscle reactivity significantly decreased in HG compared to other groups. The isoprenaline (receptor-mediated)-induced smooth muscle reactivity significantly decreased in HG compared to other groups. No significant difference was found in smooth muscle reactivity to papaverine (nonreceptor-mediated) among the groups. Gastric smooth muscle reactivity to KCl significantly increased in HG compared to other groups. Also, KCl-induced smooth muscle reactivity significantly increased in MG compared to CG and MC. Carbachol-induced smooth muscle reactivity significantly decreased in HG compared to MG, CG, and MC. No significant difference was observed in isoprenaline- and papaverine-induced smooth muscle reactivity among the groups.

CONCLUSION

Our findings suggest that memantine may influence esophageal and gastric smooth muscle reactivity in hydrocephalus.