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Yoshikazu Kinoshita - One of the best experts on this subject based on the ideXlab platform.

  • Nizatidine and Cisapride Increase Salivary Secretion in Rats
    Digestive Diseases and Sciences, 2004
    Co-Authors: Kyoichi Adachi, Hirofumi Fujishiro, Kenji Furuta, Tomoko Katsube, Tomoo Fujisawa, Takane Azumi, Shunji Ishihara, Yuji Amano, Yoshikazu Kinoshita
    Abstract:

    Saliva is a neurally induced solution with buffering capacity against acidic solutions. Salivation therefore plays an important role in defending the esophageal mucosa against refluxed gastric acid and is evoked by cholinergic stimulation. Both Nizatidine and cisapride are reported to increase acetylcholine concentrations in the postganglionic cholinergic synapses. We performed this study to clarify the effect of administration of Nizatidine and cisapride on salivary secretion. Eight-week-old male Sprague–Dawley rats were used for the experiments. Histamine-stimulated gastric acid secretion was measured after intraduodenal administration of Nizatidine or famotidine to determine the equipotent acid-suppressing doses. Salivary secretion was then measured for 3 hr after intraduodenal administration of Nizatidine (30 mg/kg), famotidine (3 mg/kg), or cisapride (1 mg/kg). Both Nizatidine and famotidine dose-dependently inhibited histamine-stimulated gastric acid secretion. Total salivary secretion was significantly increased by Nizatidine ( P = 0.02) and cisapride ( P = 0.02) but not by famotidine ( P = 0.50) compared with controls.

  • Nizatidine and cisapride enhance salivary secretion in humans.
    Alimentary pharmacology & therapeutics, 2002
    Co-Authors: Koji Adachi, M. Ono, Akira Kawamura, Mika Yuki, Hirofumi Fujishiro, Yoshikazu Kinoshita
    Abstract:

    Background: Salivation plays an important role in the defence of the oesophageal mucosa against gastric acidic reflux and can be evoked by cholinergic stimulation. Both Nizatidine and cisapride have been reported to increase acetylcholine concentrations in the cholinergic system. Aim: To investigate the effect of Nizatidine and cisapride on salivary secretion, salivary epidermal growth factor and bicarbonate output. Methods: The salivary volume and concentration of salivary epidermal growth factor and bicarbonate were measured after the administration of Nizatidine (150 mg), famotidine (20 mg) and cisapride (5 mg) in 30 male healthy volunteers. Results: Basal and stimulated salivary secretions were found to be increased after the administration of Nizatidine and cisapride. In contrast, salivary secretion was not increased by famotidine. Although epidermal growth factor content was not augmented, Nizatidine and cisapride administration also increased the bicarbonate output in mastication-stimulated saliva. Conclusions: Increased salivary secretion and bicarbonate output induced by Nizatidine may be useful for the treatment of patients with gastro-oesophageal reflux disease.

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

  • the bioequivalence of Nizatidine axid in two extemporaneously and one commercially prepared oral liquid formulations compared with capsule
    The Journal of Clinical Pharmacology, 2003
    Co-Authors: F. Johnson, Gregory L. Kearns, Susan M Abdelrahman, Ginette Gauthierdubois, Irving E Weston
    Abstract:

    Nizatidine (Axid) is an H2-receptor antagonist used for the treatment of acid-related gastrointestinal disorders. Given the frequency of these conditions in children and the potential for pediatric use of Nizatidine, an oral liquid dosage formulation would provide an alternative treatment option for patients unable to swallow solid oral dosage forms. This study was designed as an open-label, single-dose, four-way crossover trial to investigate the bioequivalence of 150 mg Nizatidine administered in three oral liquid formulations (a commercially prepared oral syrup, an extemporaneous solution in apple juice, and an extemporaneous suspension in infant formula) relative to the marketed capsule formulation. Twenty-four adult subjects (ages 31.2 +/- 7.5 years; weight 71.1 +/- 11.8 kg) were enrolled, and blood samples for determination of plasma Nizatidine concentrations were collected prior to drug administration and at 19 discrete intervals over a 24-hour postdose interval. Nizatidine was quantitated from plasma using a validated HPLC-MS assay, and a noncompartmental approach was used to describe Nizatidine biodisposition in all subjects. Significant treatment effects were observed for log-normalized Cmax, AUC0-n, and AUC0-infinity (p < 0.001). Further evaluation revealed that Nizatidine prepared in apple juice was markedly less bioavailable than the reference capsule, with 90% confidence intervals (CIs) of 0.518-0.626, 0.682-0.751, and 0.696-0.763 for Cmax, AUC0-n, and AUC0-infinity, respectively. The remaining two oral formulations demonstrated 90% CI within the guidelines established by the Food and Drug Administration (e.g., 0.80-1.25). Thus, Nizatidine in infant formula and the commercially prepared oral syrup can be considered bioequivalent to the reference capsule.

  • Pharmacokinetics and Pharmacodynamics of a Novel Nizatidine Controlled‐Release Formulation in Healthy Subjects
    Journal of clinical pharmacology, 2003
    Co-Authors: Robert A. Blum, Alan J. Braverman, Patricia Rice, F. Johnson
    Abstract:

    The pharmacokinetics and intragastric pH effects of a novel Nizatidine controlled-release (CR) formulation were compared to a currently marketed immediate-release (IR) Nizatidine formulation (Axid®). The bimodal pulsatile release characteristics of Nizatidine CR decreased its C max by approximately 42% compared to Nizatidine IR while maintaining 90% relative bioavailability; t max was approximately 1.6 times longer with the CR formulation. These characteristics enabled controlled-release Nizatidine to sustain effective plasma drug concentrations for a greater duration than immediate-release Nizatidine over the dosing intervals. In multiple doses, the 24-hour A UC ratio for all comparisons of Nizatidine CR 150 mg bid, Nizatidine CR 300 mg daily, and Nizatidine IR 150 mg bid was between 97% and 99%. Mean pH A UC values for Nizatidine CR 150 mg bid and Nizatidine IR 150 mg bid were similar overall during the 0- to 14-hour and 14- to 24-hour dosing intervals. For the 14- to 24-hour dosing interval, Nizatidine CR 150 mg maintained gastric pH over 3.0 and 4.0 for 42% and 27% of the time compared to 39% and 23% for Nizatidine IR, respectively. Nizatidine CR 300 mg, compared to the 150-mg CR and IR regimens, had a greater effect on increasing evening intragastric pH, th us providing support for the potential utility of Nizatidine CR 300 mg dosed at night in alleviating nocturnal symptoms of gastroesophageal reflux disease.

  • pharmacokinetics and pharmacodynamics of a novel Nizatidine controlled release formulation in healthy subjects
    The Journal of Clinical Pharmacology, 2003
    Co-Authors: Robert A. Blum, Alan J. Braverman, Patricia Rice, F. Johnson
    Abstract:

    The pharmacokinetics and intragastric pH effects of a novel Nizatidine controlled-release (CR) formulation were compared to a currently marketed immediate-release (IR) Nizatidine formulation (Axid®). The bimodal pulsatile release characteristics of Nizatidine CR decreased its C max by approximately 42% compared to Nizatidine IR while maintaining 90% relative bioavailability; t max was approximately 1.6 times longer with the CR formulation. These characteristics enabled controlled-release Nizatidine to sustain effective plasma drug concentrations for a greater duration than immediate-release Nizatidine over the dosing intervals. In multiple doses, the 24-hour A UC ratio for all comparisons of Nizatidine CR 150 mg bid, Nizatidine CR 300 mg daily, and Nizatidine IR 150 mg bid was between 97% and 99%. Mean pH A UC values for Nizatidine CR 150 mg bid and Nizatidine IR 150 mg bid were similar overall during the 0- to 14-hour and 14- to 24-hour dosing intervals. For the 14- to 24-hour dosing interval, Nizatidine CR 150 mg maintained gastric pH over 3.0 and 4.0 for 42% and 27% of the time compared to 39% and 23% for Nizatidine IR, respectively. Nizatidine CR 300 mg, compared to the 150-mg CR and IR regimens, had a greater effect on increasing evening intragastric pH, th us providing support for the potential utility of Nizatidine CR 300 mg dosed at night in alleviating nocturnal symptoms of gastroesophageal reflux disease.

  • Single-dose pharmacokinetics of Nizatidine (Axid) in children.
    Journal of clinical pharmacology, 2002
    Co-Authors: Susan M. Abdel-rahman, F. Johnson, Neil Manowitz, Gregory B. Holmes, Gregory L. Kearns
    Abstract:

    The pharmacokinetics of Nizatidine following a single 5.0 mg/kg oral dose given as an extemporaneous liquid formulation in apple juice was examined in 12 healthy children (8.0 +/- 2.4 years, 30.7 +/- 8.4 kg). Nizatidine and N-desmethylNizatidine were quantitated by HPLC/MS from five post dose blood samples taken over a 12-hour period. The apparent terminal elimination rate constant for Nizatidine in the pediatric subjects (0.58 +/- 0.8h(-1)) was virtually identical to that (0.54 +/- 0.13 h(-1)) previously reported from adult studies. When corrected for an estimated 30% reduction in Nizatidine oral bioavailability observed in adults upon coingestion of the drug with other fruit/vegetable juices, Nizatidine pharmacokinetic parameter estimates (e.g., Cmax, CL/F, Vss/F) in our pediatric subjects were similar to those previously reported in adults who were administered dimensionally similar (e.g., approximately 4 mg/kg) solid oral doses of the drug. Examination of the mean area under the curve (i.e., AUC0-infinity for Nizatidine and N-desmethylNizatidine suggested an approximate 15% metabolic conversion of the parent drug. Finally, Nizatidine plasma concentrations in pediatric patients following a single 5.0 mg/kg oral dose exceeded the EC50 value of the drug for gastric acid suppression determined from adult studies for approximately 6 hours.

Walter W. Offen - One of the best experts on this subject based on the ideXlab platform.

  • Nizatidine versus placebo in gastroesophageal reflux disease
    Digestive diseases and sciences, 1992
    Co-Authors: Michelle L. Cloud, Walter W. Offen
    Abstract:

    In a randomized, multicenter trial, Nizatidine 150 mg or 300 mg, or placebo, was administered twice daily for six weeks to 515 patients with gastroesophageal reflux disease (GERD). Gelusil antacid tablets were taken as needed for pain. Significantly superior rates of endoscopically proven complete healing (normal-appearing mucosa) versus placebo occurred after three weeks with Nizatidine 150 mg, and after six weeks with Nizatidine 300 mg. Six-week healing rates were 38.5% for Nizatidine 300 mg, 41.1% for Nizatidine 150 mg, and 25.8% for placebo. The Nizatidine 150 mg treatment group had significantly greater improvement in daytime and nighttime heartburn severity after one day of therapy versus placebo. Twice-daily administration of Nizatidine 150 mg or 300 mg provides prompt relief from the major symptom of GERD, heartburn, and complete healing of esophagitis is seen in many patients.

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

  • Bicarbonate stimulatory action of Nizatidine, a histamine H(2)-receptor antagonist, in rat duodenums.
    Journal of physiology Paris, 2001
    Co-Authors: H Mimaki, S Kawauchi, S Kagawa, S Ueki, K Takeuchi
    Abstract:

    Nizatidine, a histamine H(2)-antagonist, is known to inhibit acetylcholinesterase (AChE) activity and is used clinically as a gastroprokinetic agent as well as the anti-ulcer agent. We examined whether or not Nizatidine stimulates duodenal HCO(3)(-) secretion in rats through vagal-cholinergic mechanisms by inhibiting AChE activity. Under pentobarbital anesthesia, a proximal duodenal loop was perfused with saline, and the HCO(3)(-) secretion was measured at pH 7.0 using a pH-stat method and by adding 10 mM HCl. Nizatidine, neostigmine, carbachol, famotidine or ranitidine was administered i.v. as a single injection. Intravenous administration of Nizatidine (3-30 mg/kg) dose-dependently increased the HCO(3)(-) secretion, and the effect at 10 mg/kg was equivalent to that obtained by carbachol at 0.01 mg/kg. The HCO(3)(-) stimulatory action of Nizatidine was observed at the doses that inhibited the histamine-induced acid secretion and enhanced gastric motility. This effect was mimicked by neostigmine (0.03 mg/kg) and significantly attenuated by bilateral vagotomy and pretreatment with atropine but not indomethacin. The IC(50) of Nizatidine for AChE of rat erythrocytes was 1.4 x 10(-6) M, about 12 times higher than that of neostigmine. Ranitidine showed the anti-AchE activity and increased duodenal HCO(3)(-) secretion, similar to Nizatidine, whereas famotidine had any influence on neither AChE activity nor the HCO(3)(-) secretion. On the other hand, duodenal damage induced by acid perfusion (100 mM HCl for 4 h) in the presence of indomethacin was significantly prevented by Nizatidine and neostigmine, at the doses that increased the HCO(3)(-) secretion. These results suggest that Nizatidine increases HCO(3)(-) secretion in the rat duodenum, mediated by vagal-cholinergic mechanism, the action being associated with the anti-AChE activity of this agent.

  • Bicarbonate stimulatory action of Nizatidine, a histamine H2-receptor antagonist, in rat duodenums
    Journal of Physiology-paris, 2001
    Co-Authors: H Mimaki, Shigeru Ueki, S Kawauchi, S Kagawa, K Takeuchi
    Abstract:

    Abstract Nizatidine, a histamine H 2 -antagonist, is known to inhibit acetylcholinesterase (AChE) activity and is used clinically as a gastroprokinetic agent as well as the anti-ulcer agent. We examined whether or not Nizatidine stimulates duodenal HCO 3 − secretion in rats through vagal-cholinergic mechanisms by inhibiting AChE activity. Under pentobarbital anesthesia, a proximal duodenal loop was perfused with saline, and the HCO 3 − secretion was measured at pH 7.0 using a pH-stat method and by adding 10 mM HCl. Nizatidine, neostigmine, carbachol, famotidine or ranitidine was administered i.v. as a single injection. Intravenous administration of Nizatidine (3–30 mg/kg) dose-dependently increased the HCO 3 − secretion, and the effect at 10 mg/kg was equivalent to that obtained by carbachol at 0.01 mg/kg. The HCO 3 − stimulatory action of Nizatidine was observed at the doses that inhibited the histamine-induced acid secretion and enhanced gastric motility. This effect was mimicked by neostigmine (0.03 mg/kg) and significantly attenuated by bilateral vagotomy and pretreatment with atropine but not indomethacin. The IC 50 of Nizatidine for AChE of rat erythrocytes was 1.4×10 −6 M, about 12 times higher than that of neostigmine. Ranitidine showed the anti-AchE activity and increased duodenal HCO 3 − secretion, similar to Nizatidine, whereas famotidine had any influence on neither AChE activity nor the HCO 3 − secretion. On the other hand, duodenal damage induced by acid perfusion (100 mM HCl for 4 h) in the presence of indomethacin was significantly prevented by Nizatidine and neostigmine, at the doses that increased the HCO 3 − secretion. These results suggest that Nizatidine increases HCO 3 − secretion in the rat duodenum, mediated by vagal-cholinergic mechanism, the action being associated with the anti-AChE activity of this agent.

David B Allison - One of the best experts on this subject based on the ideXlab platform.

  • Nizatidine for prevention of weight gain with olanzapine a double blind placebo controlled trial
    European Neuropsychopharmacology, 2003
    Co-Authors: P Cavazzoni, Yoko Tanaka, Suraja M Roychowdhury, Alan Breier, David B Allison
    Abstract:

    Weight gain is associated with treatment with olanzapine and other psychotropic agents. Nizatidine, a histamine H-2 receptor antagonist, has been proposed to have weight-reducing effects. This double-blind trial evaluated the efficacy of Nizatidine in limiting weight gain in patients with schizophrenia and related disorders who were treated with olanzapine for up to 16 weeks. After an initial screening period, 175 patients were randomized to receive olanzapine (5-20 mg) with either placebo or Nizatidine (150 mg b.i.d. or 300 mg b.i.d.). Significantly less weight gain was observed on average at weeks 3 and 4 with olanzapine+Nizatidine 300 mg b.i.d. (P<0.05) compared to olanzapine+placebo, but the difference was not statistically significant at 16 weeks. Nizatidine was well-tolerated and did not adversely affect clinical outcomes. Nizatidine 300 mg b.i.d. may have an early transient effect in limiting the weight gain, but this potential early effect appeared to be diminished or eliminated by 16 weeks.

  • Nizatidine for prevention of weight gain with olanzapine: a double-blind placebo-controlled trial
    European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology, 2003
    Co-Authors: P Cavazzoni, Yoko Tanaka, Suraja M Roychowdhury, Alan Breier, David B Allison
    Abstract:

    Weight gain is associated with treatment with olanzapine and other psychotropic agents. Nizatidine, a histamine H-2 receptor antagonist, has been proposed to have weight-reducing effects. This double-blind trial evaluated the efficacy of Nizatidine in limiting weight gain in patients with schizophrenia and related disorders who were treated with olanzapine for up to 16 weeks. After an initial screening period, 175 patients were randomized to receive olanzapine (5-20 mg) with either placebo or Nizatidine (150 mg b.i.d. or 300 mg b.i.d.). Significantly less weight gain was observed on average at weeks 3 and 4 with olanzapine+Nizatidine 300 mg b.i.d. (P