effects of chronic consumption of heroin on basal and vagal electrical-stimulated gastric acid and pepsin secretion in rat

Addiction to opium and heroin is not only an important social and individual problem in the world but it also affects the human physiology and multiple systems. The aim of this study is to determine the effects of chronic heroin consumption on basal and vagus electrical-stimulated total gastric acid and pepsin secretion in rats. The study was carried out in the Department of Physiology, Kerman University of Medical Sciences, Iran from August 2002 to June 2003. Both male and female rats weighing 200-250g were used. Rats received daily doses of heroin intraperitoneally starting from 0.2 mg/kg to 0.1mg/kg/day up to the maintenance level of 0.7mg/kg and continued until day 12. After anesthesia, tracheotomy and laparotomy, gastric effluents were collected by washout technique with a 15 minutes interval. The total titrable acid was measured by manual titrator, and the total pepsin content was measured by Anson's method. Vagal electrical stimulation was used to stimulate the secretion of acid and pepsin. Heroin results in a significant decrease in total basal acid and pepsin secretions [4.10 +/- 0.18mmol/15 minutes versus 2.40 +/- 0.16mmol/15 minutes for acid, p<0.01, and 3.63 +/- 0.18 mg/15 minutes versus 3.11 +/- 0.18 mg/15 minutes for pepsin, p<0.05]. But, it does not produce any significant changes in acid and pepsin secretions in vagotomized condition. Heroin also causes a significant decrease in vagal-electrically stimulated acid and pepsin secretions [14.70 +/- 0.54 mmol/15 minutes versus 4.30 +/- 0.21mmol/15 minutes for acid, p<0.01, and 3.92 +/- 0.16 mg/15 minutes versus 3.37 +/- 0.16 mg/15 minutes for pepsin, p less than 0.05]. Heroin consumption decreases the total gastric basal and vagus stimulation of acid and pepsin secretion, but not in vagotomized condition. Heroin may decrease acid secretion by inhibiting vagal release of acetylcholine within the gastric wall. Other probable mechanisms include: presynaptic inhibition of acetylcholine release or depressing the vagal center, inhibition of pentagastrin induced acid secretion, inhibitory effects via central mechanisms, probably mediated by the opiate receptors. Further studies are needed to recognize the actual mechanism

Effect of thyriod hormones on basal and stimulated gastric acid secretion due to histamine, carbachol and pentagastrin in rats

Thyroid hormones affect gastric acid secretion. As the mechanism of this effect has not been fully known, in this experimental study the isolated gastric acid secretion of hypothyroid and hyperthyroid rats were compared with control group by the administration of different doses of pentagastrin, histamine and carbachol as gastric acid secretion stimulators. This study was carried out in Ahwaz University of Medical Sciences, Ahwaz, Iran in the year 2000. Each group were consisted of 8 rats [N-mari] of both sexes with a mean weight of 246 +/- 5 grams. Hypothyroid and hyperthyroid states were induced respectively by adding methimazole [500 mg/liter] for 20 days and thyroxin [500 ug/liter] for 35 days in animals drinking water. After general anesthesia, by intraperitoneal injection of sodium thiopental [50 mg/kg body weight], celiotomy was carried out quickly. The end of esophagus was tied and a silicon tube [2-2.5 mm] was entered into the stomach via duodenum and fasted in pylor region. The stomach was isolated by cutting the esophagus proximal to the tied region and the proximal part of duodenum and put into cold serous solution. After washing the serous and mucus surfaces by serous and mucus solutions, the stomach was transferred immediately to a tissue bath containing warm serous solution [V= 40 ml, T= 370C]. Gastric acid secretion in isolated stomach stimulated by pentagastrin, carbachol and histamine was measured by wash out technique and automatic titrator. Moreover, to study the effect of thyroid hormones on gastric acid secretion a number of dose-dependent experiments after the administration of different doses of histamine [50, 100, 150, 200 umol], carbachol [50, 100, 150, 200 umol], and pentagastrin [30, 60, 90, 120 ug/kg body weight] were performed. Both basal and histamine, carbachol, pentagastrin stimulated-acid secretion decreased and increased in hypothyroid and hyperthyroid groups compared with control group. It seems that thyroid hormones have not exert their effects by changing the cholinergic, gastrin and histamine receptors but probably by alerting the number or size of the secretory cells in stomach