ABSTRACT
Abdominal colic, constipation and delay in gastric emptying are symptoms of lead poisoning, but there is scant information about the effect of lead on gastric motility. In the present study, we investigated the effect of lead acetate on gastric motility in rats. Animals were divided into nine groups [n=8]; four groups were exposed to lead acetate solution [1%] for 1, 2, 3, and 4 weeks [Pb1, Pb2, Pb3, and Pb4 groups, respectively]. Sodium acetate solution was given to another four groups for 1, 2, 3, and 4 weeks [Na1, Na2, Na3, and Na4 groups, respectively] and the control group had free access to tap water. Gastric motility was measured in the basal and acetylcholine [Ach]-stimulated states using a physiograph instrument. Nitric oxide metabolite of gastric tissue was determined by Griess micro-assay. There were no significant differences between basal and Ach-stimulated gastric motility in Pb1, Pb2, Na1, and Na2 groups. However, it was significantly greater in Pb3 and Pb4 groups when compared with Na3 and Na4 groups in both basal and Ach-stimulated states [P<0.05]. In addition, nitric oxide metabolite of gastric tissue was more in all Pb groups in comparison with their Na counterparts [P<0.05]. We found that lead exposure could affect gastric motility via the nitric oxide pathway