Lead exposure changes gastric acid secretion in rat: role of nitric oxide [No]

Sub chronic exposure to lead in rats slows gastric emptying, but little is known about the effects of lead on gastric secretion. This study was designed to investigate the effects of lead on gastric acid secretion and its possible mechanisms in rats. Lead acetate was dissolved in drinking water in a concentration of 1%. Sodium acetate-containing water with a molar concentration similar to lead was also prepared. We had nine groups of animals [n=8]; four of them were exposed to lead for 1, 2, 3, and 4 weeks [Pbl, Pb2, Pb3 and Pb4 groups, respectively]. Sodium acetate solution was given to another four groups for 1, 2, 3, and 4 weeks [Nal, Na2, Na3 and Na4 groups, respectively]. Gastric secretion was collected by washout technique and its acid output was measured in the basal [Basal Acid Output, BAO], vogotomy [Vagotomized Acid Output, VAO], and vagally stimulated [Vagally Stimulated Acid Output, VSAO] states using titrator instrument. Nitric oxide [NO] metabolite of gastric tissue was determined by Griess micro assay method to evaluate the possible mechanism of lead effect on gastric secretion. VSAO was significantly less in Pbl and Pb2 groups than Nal and Na2 ones respectively [1.75 +/- 0.17, 2.10 +/- 0.30 vs. 5.79 +/- 0.20, 6.18 +/- 0.27 micromol/15min] [P=0.001, P=0.001] BAO was significantly more in Pb3 and Pb4 groups than Na3 and Na4 ones respectively [2.77 +/- 0.37, 2.80 +/- 0.31 vs. 1.73 +/- 0.16, 1.79 +/- 0.34 micromol/15min] [P=0.01, P=0.02], but it was the same after vagotomy. VSAO was more in Pb3 and Pb4 groups than their Na counterparts [P=0.001, P=0.0001] NO metabolite of gastric tissue was more in all Pb groups in comparison to their Na counterparts [P=0.0001]. In this study, it seems that lead exposure, via NO mechanism, has different effects on acid secretion. Nitric oxide in small and large amounts decrease and increase gastric acid secretion, respectively

effect of acute consumption of paraoxon on basal and Pentagastrin-Stimulated Gastric acid and pepsin secretion in rats

Paraoxon is an organophosphate. Organophosphate inhibit acetylcholinestrase enzyme and cause nicotinic and muscarinic sings. There is no study on our knowledge regarding the effect of these substances on gastric acid and pepsin secretion. In the present study, the effect of acute consumption of paraoxon on gastric acid and pepsin secretion has been investigated. In the present study 30 female N-mari rats weighing 200-250gr were used. The first group [paraoxon] received 0.5mg/kg paraoxon intraperitonealy. The second group [alcohol] received the dozes of ethyl alcohol [96%] and the third group [control] received no drug. Animals were anesthetized by intraperitoneal injection of 50mg/kg Sodium thiopental. After trachesotomy and laparatomy gastric secretions were collected with a tube via duodenum. Pentagastrin [25 micro g/kg. ip] was used as gastric stimulator. Acid and pepsin secretions were measured by titration and Anson methods respectively. Stages of measurement were basal, stimulated. and re-basal. The basal acid secretion in control, alcohol and paraoxon groups was 7.6 +/- 0.26, 7.46 +/- 0.4 and 7.03 +/- 0.28 micro mol/15min respectively that shows no significant difference among three groups. Although following pentagastrin-stimulation acid secretion was significantly more than basal stage in all groups, but there was significantly more secretion in control than alcohol subjects. But there was no difference between control and paraoxon or alcohol and paraoxon groups in this regard. Regarding pepsin secretion, there was significantly more secretion in alcohol subjects than others in all measured stages. In comparison to control group, acute paraoxon has no effect on basal acid pepsin secretion, while acute alcohol caused a significant increase in basal acid/pepsin secretion