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Fatemeh Nabavizadeh Rafsanjani - One of the best experts on this subject based on the ideXlab platform.

  • 1 THE EFFECT OF ACUTE CONSUMPTION OF PARAOXON ON BASAL AND PENTAGASTRIN-STIMULATED GASTRIC ACID AND Pepsin Secretion IN RATS
    2015
    Co-Authors: Pak J Physiol, Fatemeh Nabavizadeh Rafsanjani, Jalal Vahedian, Zakieh Vahedian Ardakani, Mehran Moradi, Amir Fakhr Attar
    Abstract:

    enzy me 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. Methods: 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 (25µg/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. Results: The basal acid Secretion in control, alcohol and paraoxon groups was 7.6±0.26, 7.46±0.4 and 7.03±0.28µmol/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. Conclusion: 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

  • the effects of chronic consumption of heroin on basal and vagal electrical stimulated gastric acid and Pepsin Secretion in rat
    Saudi Medical Journal, 2004
    Co-Authors: Fatemeh Nabavizadeh Rafsanjani, Jalal Vahedian, Fatemeh Maghouli, F. Esmaeili
    Abstract:

    OBJECTIVES 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. METHODS 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 200-250 g were used. Rats received daily doses of heroin intraperitoneally starting from 0.2 mg/kg to 0.1 mg/kg/day up to the maintenance level of 0.7 mg/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. RESULTS Heroin results in a significant decrease in total basal acid and Pepsin Secretions (4.10 +/- 0.18 mmol/15 minutes versus 2.40 +/- 0.16 mmol/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 +/- 0.21 mmol/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<0.05). CONCLUSIONS 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.

  • The effect of insulin-dependent diabetes mellitus on basal and distention-induced acid and Pepsin Secretion in rat.
    Diabetes research and clinical practice, 2004
    Co-Authors: Fatemeh Nabavizadeh Rafsanjani, Jalal Vahedian
    Abstract:

    Abstract Background: Diabetes mellitus is one of the most common endocrine diseases and affects most body organs. It affects gastric acid Secretion, but this effect has not been fully understood. As the effects of diabetes on gastric Pepsin Secretion has not been proved yet, in this experimental study basal and distension-stimulated acid and Pepsin Secretions of diabetic and non-diabetic rats have been compared. Material and methods: Female N-Mari rats weighing 200–250g were used. Diabetic state was induced by intraperitoneal injection of 75mg/kg streptozotocin. Animals were anaesthetized by the interaperitoneal injection of 60mg/kg thiopental sodium. Then tracheostomy and laparotomy were done and gastric Secretions were collected by a cannula entered via duodenum. Gastric distention induce by 1.5ml normal saline per each 100g of body weight in stomach. Acid and Pepsin were measured by titration and Anson's method, respectively. Results: Basal gastric Secretions were similar in diabetic and non-diabetic animals. Distention-stimulated acid Secretions in diabetic and non-diabetic rats were 3.24±0.16 and 8.05±0.21μmol/15min, respectively, which were significantly different ( P =0.00001). Distention-induced Pepsin Secretion in diabetic and non diabetic rats were 3.16±0.13 and 5.24±0.16μg/15min, respectively, which were significantly different ( P =0.00001). Conclusion: In this study the stomach of diabetic animals showed less reaction to distention, which may be due to the reduction of acid and Pepsin secretary cells, reduction of the function of the cells, gastric atrophy or gastric vagus neuropathy. These probabilities need to be examined.

  • The effects of chronic consumption of heroin on basal and vagal electrical-stimulated gastric acid and Pepsin Secretion in rat.
    Saudi medical journal, 2004
    Co-Authors: Fatemeh Nabavizadeh Rafsanjani, Jalal Vahedian, Fatemeh Maghouli, F. Esmaeili
    Abstract:

    OBJECTIVES 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. METHODS 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 200-250 g were used. Rats received daily doses of heroin intraperitoneally starting from 0.2 mg/kg to 0.1 mg/kg/day up to the maintenance level of 0.7 mg/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. RESULTS Heroin results in a significant decrease in total basal acid and Pepsin Secretions (4.10 +/- 0.18 mmol/15 minutes versus 2.40 +/- 0.16 mmol/15 minutes for acid, p

  • THE EFFECTS OF ACUTE CONSUMPTION OF HEROIN ON BASAL AND VAGAL-STIMULATED GASTRIC ACID AND Pepsin Secretion IN RAT
    Iranian Journal of Medical Sciences, 2003
    Co-Authors: Fatemeh Nabavizadeh Rafsanjani, Adel Najafi, F. Esmaeili
    Abstract:

    Background: Opioid peptides and their receptors are present in the majority of body tissues including gastrointestinal tract. Heroin is one of the opioid derivatives that abuse increasingly today. So far, there is no study on the effect of acute heroin administration on gastric acid and Pepsin Secretion. Objective: To define the effect of the acute heroin consumption on basal and vagal-stimulated gastric acid and Pepsin Secretion in rat. Methods: Pure heroin (0.5 mg/kg, ip) was injected to 24 rats. After confirming the signs of heroin effect, animals were anesthetized with sodium thiopental (60 mg/kg, ip). Then, tracheostomy and laparotomy were done, gastric contents were collected by wash out technique over 15 min. The total titrable acid was measured by acid titrator. The Pepsin content was measured by Anson method. Vagal electrical stimulation was used to stimulate the Secretion of acid and Pepsin. Results: A significant increase in both basal and vagotomized state of gastric acid Secretion in that group that received heroin, as compared to the control group was shown. Also, in comparison to the control group, electrical stimulation of vagus nerve increased the gastric acid Secretion in animals that received heroin. This change, however, was not significant. The basal and vagally stimulated Secretion of Pepsin was increased, though not significantly, in heroin group in comparison to control group.

Jalal Vahedian - One of the best experts on this subject based on the ideXlab platform.

  • 1 THE EFFECT OF ACUTE CONSUMPTION OF PARAOXON ON BASAL AND PENTAGASTRIN-STIMULATED GASTRIC ACID AND Pepsin Secretion IN RATS
    2015
    Co-Authors: Pak J Physiol, Fatemeh Nabavizadeh Rafsanjani, Jalal Vahedian, Zakieh Vahedian Ardakani, Mehran Moradi, Amir Fakhr Attar
    Abstract:

    enzy me 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. Methods: 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 (25µg/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. Results: The basal acid Secretion in control, alcohol and paraoxon groups was 7.6±0.26, 7.46±0.4 and 7.03±0.28µmol/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. Conclusion: 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

  • THE EFFECT OF ACUTE CONSUMPTION OF PARAOXON ON BASAL AND PENTAGASTRIN-STIMULATED GASTRIC ACID AND Pepsin Secretion IN RATS
    2006
    Co-Authors: Fatemeh Nabavizadeh, Jalal Vahedian, Zakieh Vahedian Ardakani, Mehran Moradi
    Abstract:

    Background: Paraoxon is an organophosphate. Organophosphates inhibit acetylcholinestrase enzy me 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. Methods: 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 (25μg/kg, ip) was used as gastric stimulator. Acid and Pepsin Secretions were measured bytitration and Anson methods respectively. Stages of measurement were basal, stimulated, and rebasal. Results: The basal acid Secretion in control, alcohol and paraoxon groups was 7.6±0.26, 7.46±0.4 and 7.03±0.28μmol/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. Conclusion: in comparison to control group, acute paraoxon has no effect on basal acid/Pepsin Secretion,

  • the effects of chronic consumption of heroin on basal and vagal electrical stimulated gastric acid and Pepsin Secretion in rat
    Saudi Medical Journal, 2004
    Co-Authors: Fatemeh Nabavizadeh Rafsanjani, Jalal Vahedian, Fatemeh Maghouli, F. Esmaeili
    Abstract:

    OBJECTIVES 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. METHODS 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 200-250 g were used. Rats received daily doses of heroin intraperitoneally starting from 0.2 mg/kg to 0.1 mg/kg/day up to the maintenance level of 0.7 mg/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. RESULTS Heroin results in a significant decrease in total basal acid and Pepsin Secretions (4.10 +/- 0.18 mmol/15 minutes versus 2.40 +/- 0.16 mmol/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 +/- 0.21 mmol/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<0.05). CONCLUSIONS 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.

  • The effect of insulin-dependent diabetes mellitus on basal and distention-induced acid and Pepsin Secretion in rat.
    Diabetes research and clinical practice, 2004
    Co-Authors: Fatemeh Nabavizadeh Rafsanjani, Jalal Vahedian
    Abstract:

    Abstract Background: Diabetes mellitus is one of the most common endocrine diseases and affects most body organs. It affects gastric acid Secretion, but this effect has not been fully understood. As the effects of diabetes on gastric Pepsin Secretion has not been proved yet, in this experimental study basal and distension-stimulated acid and Pepsin Secretions of diabetic and non-diabetic rats have been compared. Material and methods: Female N-Mari rats weighing 200–250g were used. Diabetic state was induced by intraperitoneal injection of 75mg/kg streptozotocin. Animals were anaesthetized by the interaperitoneal injection of 60mg/kg thiopental sodium. Then tracheostomy and laparotomy were done and gastric Secretions were collected by a cannula entered via duodenum. Gastric distention induce by 1.5ml normal saline per each 100g of body weight in stomach. Acid and Pepsin were measured by titration and Anson's method, respectively. Results: Basal gastric Secretions were similar in diabetic and non-diabetic animals. Distention-stimulated acid Secretions in diabetic and non-diabetic rats were 3.24±0.16 and 8.05±0.21μmol/15min, respectively, which were significantly different ( P =0.00001). Distention-induced Pepsin Secretion in diabetic and non diabetic rats were 3.16±0.13 and 5.24±0.16μg/15min, respectively, which were significantly different ( P =0.00001). Conclusion: In this study the stomach of diabetic animals showed less reaction to distention, which may be due to the reduction of acid and Pepsin secretary cells, reduction of the function of the cells, gastric atrophy or gastric vagus neuropathy. These probabilities need to be examined.

  • The effects of chronic consumption of heroin on basal and vagal electrical-stimulated gastric acid and Pepsin Secretion in rat.
    Saudi medical journal, 2004
    Co-Authors: Fatemeh Nabavizadeh Rafsanjani, Jalal Vahedian, Fatemeh Maghouli, F. Esmaeili
    Abstract:

    OBJECTIVES 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. METHODS 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 200-250 g were used. Rats received daily doses of heroin intraperitoneally starting from 0.2 mg/kg to 0.1 mg/kg/day up to the maintenance level of 0.7 mg/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. RESULTS Heroin results in a significant decrease in total basal acid and Pepsin Secretions (4.10 +/- 0.18 mmol/15 minutes versus 2.40 +/- 0.16 mmol/15 minutes for acid, p

Basil I. Hirschowitz - One of the best experts on this subject based on the ideXlab platform.

  • long term lansoprazole control of gastric acid and Pepsin Secretion in ze and non ze hypersecretors a prospective 10 year study
    Alimentary Pharmacology & Therapeutics, 2001
    Co-Authors: Basil I. Hirschowitz, J Simmons, Jean Mohnen
    Abstract:

    Background: The majority of patients with Zollinger–Ellison syndrome require lifelong treatment with proton pump inhibitors. Aims: To determine the efficacy of lansoprazole control of acid and Pepsin Secretion over the long term in Zollinger–Ellison syndrome and non-Zollinger–Ellison syndrome hypersecretors. Methods: Sixty-three hypersecretors (basal acid output > 15 mmol/h), 46 Zollinger–Ellison syndrome and 17 non-Zollinger–Ellison syndrome, with a total history of 15.4 and 19.2 years, respectively, were entered into a long-term prospective study using lansoprazole. Sixty-one were studied every 3 months for 1 year and then every 3–6 months up to 10 years during lansoprazole treatment with endoscopy, serum gastrin and gastric analysis, measuring both basal and stimulated pH and acid and Pepsin Secretion. Doses were individually optimized and adjusted to keep the basal acid output at < 5 mmol/h in intact patients and < 1 mmol/h in antrectomized Zollinger–Ellison syndrome patients. Results: The dose of lansoprazole could not be predicted a priori from pre-treatment acid or Pepsin output, serum gastrin, prior omeprazole dose or diagnosis or prior complications. The median dose was ∼ 80 mg/day, with a wide range from 15 mg every other day to 360 mg/day, and generally stabilized by 12 months. However, as doses were adjusted over time for indications, almost half the patients required higher doses. With adjustments, the basal acid output was maintained in the target range in > 90% of intact patients and in 80% of antrectomized patients. Gastric juice pH increased from ∼ 1.2 before therapy to > 3.4 during therapy. Serum gastrin in Zollinger–Ellison syndrome patients, after excluding five outliers, did not change over the course of therapy, but doubled in non-Zollinger–Ellison syndrome patients. There were no adverse events due to lansoprazole, and routine laboratory studies remained normal. Conclusions: The dose of lansoprazole for hypersecretors cannot be predicted, and thus needs to be optimized empirically on an individual basis. With continued periodic adjustments, almost half the patients required increased doses, while safe dose reduction was possible in only one-quarter. When individually optimized, lansoprazole proved to be safe and effective in the control of Secretion for the treatment of both Zollinger–Ellison syndrome and non-Zollinger–Ellison syndrome hypersecretors for up to 10 years.

  • a critical analysis with appropriate controls of gastric acid and Pepsin Secretion in clinical esophagitis
    Gastroenterology, 1991
    Co-Authors: Basil I. Hirschowitz
    Abstract:

    Abstract Because esophagitis is a presumed "acid-peptic" disease, fasting gastric contents (volume and acid and Pepsin concentrations) and basal and pentagastrin-stimulated acid and Pepsin outputs were studied in 155 patients with endoscopically defined (and graded 1–4) esophagitis and 508 control patients without esophagitis. Basal Pepsin and maximal acid and Pepsin outputs were lower in the patients with esophagitis than in those without esophagitis. In further analysis, the patients were subdivided into three categories, duodenal ulcer, nonulcer with no disease other than esophagitis, and postgastric surgery, because these categories affect gastric Secretion independently of esophageal disease and in the rank order given. Each category was subdivided by sex, because men secreted more than women. Within each category there was no systematic difference in fasting, basal, or maximal gastric acid or Pepsin Secretion between patients with and patients without esophagitis. Severity of esophagitis was not related to any Secretion parameters. Hiatal hernia was present in 50% of patients with esophagitis vs. 15% of controls without the condition ( P 10 mm Hg had esophagitis. Because neither the composition of gastric juice nor basal or stimulated gastric acid or Pepsin output could be correlated to the presence or severity of esophagitis, factors other than amount or composition of gastric juice per se must be responsible for susceptibility to esophagitis.

Koji Takeuchi - One of the best experts on this subject based on the ideXlab platform.

  • 928 modulation by muscarinic acetylcholine receptor subtype 4 of carbachol induced Pepsin Secretion in mice relation to d cells somatostatin
    Gastroenterology, 2008
    Co-Authors: Nobuaki Takahashi, Takuya Endo, Kikuko Amagase, Eiji Nakamura, Susumu Okabe, Minoru Matsui, Koji Takeuchi
    Abstract:

    Background/Aim: Muscarinic acetylcholine receptors (mAChRs) consist of five subtypes (M1~M5) and are widely expressed to mediate diverse autonomic functions in peripheral organs, including the gastrointestinal tract. Although both M1and M3receptors reportedly play a role in the regulation of Pepsin Secretion in response to acetylcholine, we recently found that carbachol (CCh)-induced Pepsin Secretion wasmarkedly decreased inM4 knockout (KO) mice. In the present study, we demonstrated, using M1~M5 KO mice, the importance of M4 receptors in the cholinergic regulation of Pepsin Secretion and investigated how this Secretion is modulated by the activation of M4 receptors. Methods: C57BL/6J mice of wildtype (WT) and M1-, M2-, M3-, M4or M5-KO were used. Under urethane anesthesia, the abdomen was incised, the cardiac portion was ligated, and an acute fistula prepared with a polyethylene tube was provided in the stomach through a pylorus. Then, the stomach was instilled with saline (0.4 ml) through the fistula, and the solution was changed every 20 min. CCh (30 μg/kg) was given SC as a single injection. Atropine (0.3 mg/kg) or CYN154806 [somatostatin-2 receptor (SST2R) antagonist 0.1-3mg/kg] was given SC 20 min before CCh. Expressions of D cells and M4 receptors were examined immunohistochemically by double staining with anti-somatostatin and anti-M4 receptor antibodies. Results: CCh caused an increase of Pepsin Secretion in WT mice, and the effect was completely inhibited by prior administration of atropine. The stimulatory effect of CCh was similarly observed in the animals lacking M1-, M2or M5-receptors but significantly decreased in M3or M4KO mice, as compared to WT; especially, the response was all but completely abolished in M4-KOmice. CYN154806, the SST2R antagonist, significantly reversed the decreased Pepsin response to CCh in M4but not M3-KO mice. The M4-KO mice showed basal Pepsin Secretion much less than WT mice, and these changes were also reversed by CYN154806. By contrast, somatostatin decreased Pepsin Secretion under basal and CCh-stimulated conditions. Furthermore, the immunohistochemical study showed the localization ofM4 receptors on D cells in the mouse stomach. Conclusion: These results suggest that under cholinergic stimulation the Secretion of Pepsin is mediated mainly by the activation of M4-receptors and partly through M3-receptors but does not involve other muscarinic receptor subtypes. Somatostatin has an inhibitory effect on Pepsin Secretion through SST2 receptors. It is assumed that the activation of M4-receptors inhibits the release of somatostatin from D cells and results in enhancement of Pepsin response.

  • 928 Modulation By Muscarinic Acetylcholine Receptor Subtype 4 of Carbachol- Induced Pepsin Secretion in Mice: Relation to D Cells/Somatostatin
    Gastroenterology, 2008
    Co-Authors: Nobuaki Takahashi, Takuya Endo, Kikuko Amagase, Eiji Nakamura, Susumu Okabe, Minoru Matsui, Koji Takeuchi
    Abstract:

    Background/Aim: Muscarinic acetylcholine receptors (mAChRs) consist of five subtypes (M1~M5) and are widely expressed to mediate diverse autonomic functions in peripheral organs, including the gastrointestinal tract. Although both M1and M3receptors reportedly play a role in the regulation of Pepsin Secretion in response to acetylcholine, we recently found that carbachol (CCh)-induced Pepsin Secretion wasmarkedly decreased inM4 knockout (KO) mice. In the present study, we demonstrated, using M1~M5 KO mice, the importance of M4 receptors in the cholinergic regulation of Pepsin Secretion and investigated how this Secretion is modulated by the activation of M4 receptors. Methods: C57BL/6J mice of wildtype (WT) and M1-, M2-, M3-, M4or M5-KO were used. Under urethane anesthesia, the abdomen was incised, the cardiac portion was ligated, and an acute fistula prepared with a polyethylene tube was provided in the stomach through a pylorus. Then, the stomach was instilled with saline (0.4 ml) through the fistula, and the solution was changed every 20 min. CCh (30 μg/kg) was given SC as a single injection. Atropine (0.3 mg/kg) or CYN154806 [somatostatin-2 receptor (SST2R) antagonist 0.1-3mg/kg] was given SC 20 min before CCh. Expressions of D cells and M4 receptors were examined immunohistochemically by double staining with anti-somatostatin and anti-M4 receptor antibodies. Results: CCh caused an increase of Pepsin Secretion in WT mice, and the effect was completely inhibited by prior administration of atropine. The stimulatory effect of CCh was similarly observed in the animals lacking M1-, M2or M5-receptors but significantly decreased in M3or M4KO mice, as compared to WT; especially, the response was all but completely abolished in M4-KOmice. CYN154806, the SST2R antagonist, significantly reversed the decreased Pepsin response to CCh in M4but not M3-KO mice. The M4-KO mice showed basal Pepsin Secretion much less than WT mice, and these changes were also reversed by CYN154806. By contrast, somatostatin decreased Pepsin Secretion under basal and CCh-stimulated conditions. Furthermore, the immunohistochemical study showed the localization ofM4 receptors on D cells in the mouse stomach. Conclusion: These results suggest that under cholinergic stimulation the Secretion of Pepsin is mediated mainly by the activation of M4-receptors and partly through M3-receptors but does not involve other muscarinic receptor subtypes. Somatostatin has an inhibitory effect on Pepsin Secretion through SST2 receptors. It is assumed that the activation of M4-receptors inhibits the release of somatostatin from D cells and results in enhancement of Pepsin response.

F. Esmaeili - One of the best experts on this subject based on the ideXlab platform.

  • the effects of chronic consumption of heroin on basal and vagal electrical stimulated gastric acid and Pepsin Secretion in rat
    Saudi Medical Journal, 2004
    Co-Authors: Fatemeh Nabavizadeh Rafsanjani, Jalal Vahedian, Fatemeh Maghouli, F. Esmaeili
    Abstract:

    OBJECTIVES 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. METHODS 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 200-250 g were used. Rats received daily doses of heroin intraperitoneally starting from 0.2 mg/kg to 0.1 mg/kg/day up to the maintenance level of 0.7 mg/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. RESULTS Heroin results in a significant decrease in total basal acid and Pepsin Secretions (4.10 +/- 0.18 mmol/15 minutes versus 2.40 +/- 0.16 mmol/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 +/- 0.21 mmol/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<0.05). CONCLUSIONS 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.

  • The effects of chronic consumption of heroin on basal and vagal electrical-stimulated gastric acid and Pepsin Secretion in rat.
    Saudi medical journal, 2004
    Co-Authors: Fatemeh Nabavizadeh Rafsanjani, Jalal Vahedian, Fatemeh Maghouli, F. Esmaeili
    Abstract:

    OBJECTIVES 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. METHODS 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 200-250 g were used. Rats received daily doses of heroin intraperitoneally starting from 0.2 mg/kg to 0.1 mg/kg/day up to the maintenance level of 0.7 mg/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. RESULTS Heroin results in a significant decrease in total basal acid and Pepsin Secretions (4.10 +/- 0.18 mmol/15 minutes versus 2.40 +/- 0.16 mmol/15 minutes for acid, p

  • THE EFFECTS OF ACUTE CONSUMPTION OF HEROIN ON BASAL AND VAGAL-STIMULATED GASTRIC ACID AND Pepsin Secretion IN RAT
    Iranian Journal of Medical Sciences, 2003
    Co-Authors: Fatemeh Nabavizadeh Rafsanjani, Adel Najafi, F. Esmaeili
    Abstract:

    Background: Opioid peptides and their receptors are present in the majority of body tissues including gastrointestinal tract. Heroin is one of the opioid derivatives that abuse increasingly today. So far, there is no study on the effect of acute heroin administration on gastric acid and Pepsin Secretion. Objective: To define the effect of the acute heroin consumption on basal and vagal-stimulated gastric acid and Pepsin Secretion in rat. Methods: Pure heroin (0.5 mg/kg, ip) was injected to 24 rats. After confirming the signs of heroin effect, animals were anesthetized with sodium thiopental (60 mg/kg, ip). Then, tracheostomy and laparotomy were done, gastric contents were collected by wash out technique over 15 min. The total titrable acid was measured by acid titrator. The Pepsin content was measured by Anson method. Vagal electrical stimulation was used to stimulate the Secretion of acid and Pepsin. Results: A significant increase in both basal and vagotomized state of gastric acid Secretion in that group that received heroin, as compared to the control group was shown. Also, in comparison to the control group, electrical stimulation of vagus nerve increased the gastric acid Secretion in animals that received heroin. This change, however, was not significant. The basal and vagally stimulated Secretion of Pepsin was increased, though not significantly, in heroin group in comparison to control group.