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Pharmaceuticals have recently emerged as a significant environmental concern due to the growth of population, expansion of industry, and the shift in modern lifestyles. Herein, we present a Fe(II)/percarbonate (SPC) process with dramatically enhanced efficiency by the introduction of zerovalent iron (ZVI). After the addition of ZVI, the removal rate of nizatidine (NZTD) went up from 71.7 to 84.2%. The removal rate of NZTD decreases with rising pH and speeds up with increasing temperature. It was found that under the condition of pH = 7 and T = 25 °C, the molar ratio of the optimal concentration of NZTD degradation in the system was [NZTD]0:[SPC]0:[Fe(II)]0:[ZVI]0 = 1:8:24:16, with a degradation rate of 99.8%. At the same time, target pollutants can also be successfully eliminated from actual water bodies. Moreover, we test for toxicity using luminescent bacteria, and the results demonstrate that the system is capable of effectively decreasing the toxicity of NZTD. The research findings can contribute to the clarification of the migration and transformation law of NZTD in the oxidation process, thereby providing a scientific basis and technical support for the removal of NZTD in the tertiary water treatment for a water source. [ABSTRACT FROM AUTHOR]

Two sensitive, simple and rapid UV and second order derivative spectrophotometric methods were developed for the determination of nizatidine and ranitidine hydrochloride in pure form and pharmaceutical preparations. For the first method, UV spectrophotometic method, nizatidine was determined at 325 nm and ranitidine at 325.5 nm with detection limits of 0.07 and 0.04 μg/mL, respectively. For the second method, the distances between two extremum values (peak-to-peak amplitudes), 328/356.5 nm for nizatidine and 326/357 nm for ranitidine were measured in the second order derivative-spectra. The detection limits were found to be 0.02 μg/mL for nizatidine and 0.016 μg/mL for ranitidine, respectively. The thermal analysis of the two drugs was studied by Thermogravimetric Analysis-Differential Scanning Calorimetry (TGA-DSC) techniques. Enthalpy changes were obtained 121.9 and 124.15 J/g for nizatidine and ranitidine, respectively. The proposed method was successfully applied to the analysis of pharmaceutical preparations. The results were in good agreement with those obtained using the reference method; no significant difference were found in the accuracy and precision as revealed by the accepted values of t- and F-tests. [ABSTRACT FROM AUTHOR]

Thermogravimetry (TG), differential scanning calorimetry (DSC), polarized light thermal microscopy (PLTM), as well as X-ray powder diffraction (XRD) and Fourier transformed infrared spectroscopy (FTIR) were used to study the thermal behavior and the chemical structure of cimetidine, famotidine, ranitidine-HCl, and nizatidine. The TG-DSC curves show that the famotidine and ranitidine-HCl suffer decomposition during melting and they are thermally less stable in comparison with cimetidine and nizatidine, the latter being the most stable of all the drugs studied in this study. The DSC curves of famotidine and ranitidine-HCl show exothermic peaks immediately after the melting, confirming the occurrence of thermal decomposition. The DSC curves also show that the cimetidine and nizatidine have some thermal stability after melting. The thermal events shown in the PLTM images are consistent with the results shown in the TG-DSC and DSC curves. The XRD patterns show that the cimetidine and famotidine are less crystalline compared with ranitidine-HCl and nizatidine. The theoretical FTIR bands are in agreement with those obtained experimentally, and in some cases, no difference is observed between the theoretical and experimental values, even being identical in one of the cases. [ABSTRACT FROM AUTHOR]

The aim of this study was to elucidate the intestinal epithelial cell efflux transport processes that are involved in the intestinal transport of the H2 receptor antagonist nizatidine. The intestinal epithelial efflux transport mechanisms of nizatidine were investigated and characterized across Caco-2 cell monolayers, in the concentration range 0.05–10 mM in both apical–basolateral (AP–BL) and BL–AP directions, and the transport constants of P-glycoprotein (P-gp) efflux activity were calculated. The concentration-dependent effects of various P-gp (verapamil, quinidine, erythromycin, ketoconazole, and cyclosporine A), multidrug resistant-associated protein 2 (MRP2; MK-571, probenecid, indomethacin, and p-aminohipuric acid), and breast cancer resistance protein (BCRP; Fumitremorgin C) inhibitors on nizatidine bidirectional transport were examined. Nizatidine exhibited 7.7-fold higher BL–AP than AP–BL Caco-2 permeability, indicative of net mucosal secretion. All P-gp inhibitors investigated displayed concentration-dependent inhibition on nizatidine secretion in both directions. The IC50 of verapamil on nizatidine P-gp secretion was 1.2 × 10−2 mM. In the absence of inhibitors, nizatidine displayed concentration-dependent secretion, with one saturable ( J max = 5.7 × 10−3 nmol∙cm−2∙s−1 and K m = 2.2 mM) and one nonsaturable component ( K d = 7 × 10−4 μL∙cm−2∙s−1). Under complete P-gp inhibition, nizatidine exhibited linear secretory flux, with a slope similar to the nonsaturable component. V max and K m estimated for nizatidine P-gp-mediated secretion were 4 × 10−3 nmol∙cm−2∙s−1 and 1.2 mM, respectively. No effect was obtained with the MRP2 or the BCRP inhibitors. Being a drug commonly used in pediatrics, adults, and elderly, nizatidine susceptibility to efflux transport by P-gp revealed in this paper may be of significance in its absorption, distribution, and clearance, as well as possible drug–drug interactions. [ABSTRACT FROM AUTHOR]

Two Spectrophotometric procedures are presented for the determination of two commonly used H2-receptor antagonists, nizatidine (I) and ranitidine hydrochloride (II). The methods are based mainly on charge transfer complexation reaction of these drugs with either ρ-chloranilic acid (ρ-CA) or 2, 3 dichloro-5, 6-dicyanoquinone (DDQ). The produced colored products are quantified spectrophotometrically at 515 and 467 nm in chloranilic acid and DDQ methods, respectively. The molar ratios for the reaction products and the optimum assay conditions were studied. The methods determine the cited drugs in concentration ranges of 20-200 and 20-160 μg/mL for nizatidine and ranges of 20-240 and 20-140 μg/mL for ranitidine with chloranilic acid and DDQ methods, respectively. A more detailed investigation of the complexes formed was made with respect to their composition, association constant, molar absorptivity and free energy change. The proposed procedures were successfully utilized in the determination of the drugs in pharmaceutical preparations. The standard addition method was applied by adding nizatidine and ranitidine to the previously analyzed tablets or capsules. The recovery of each drug was calculated by comparing the concentration obtained from the spiked mixtures with those of the pure drug. The results of analysis of commercial tablets and the recovery study (standard addition method) of the cited drugs suggested that there is no interference from any excipients, which are present in tablets or capsules. Statistical comparison of the results was performed with regard to accuracy and precision using student’s t-test and F-ratio at 95% confidence level. There is no significant difference between the reported and proposed methods with regard to accuracy and precision. [ABSTRACT FROM AUTHOR]

Background. The purpose of this study was to propose clinical and pathologic criteria for the indication for steroid therapy (ST) in adult IgA nephropathy (IgAN). Methods. We analyzed 275 adult IgAN patients retrospectively, using a histological scoring system. The histological score was expressed by evaluating, semiquantitatively, the extent of glomerular and tubulointerstitial lesions in terms of the activity index (AI) and chronicity index (CI). To determine the applicability of ST, three groups were categorized by evaluating the statistical significance of the correlation between the AI and CI, together with the daily amount of urinary protein (UP) and the outcome. Results. In group A, which had a CI ≧ 5 alone, 33 out of 43 patients showed a decline in renal function. There was no statistically significant difference between the subgroup with ST and that without ST. In group B, which had CI < 5, AI < 5, and UP < 1.0 g/day, 169 out of 174 patients had normal renal function irrespective of whether or not they received ST. Thus, ST had no beneficial effects in group A and B patients. In group C, which had CI < 5 and AI ≧ 5 or UP ≧ 1.0 g/day, patients with ST had a significantly higher incidence of an outcome with normal renal function (22 out of 24 patients) than that in patients without ST (19 out of 34 patients) (P < 0.01). Thus, ST had beneficial effects in group C patients. Conclusions. We propose that a histological criterion be used in combination with the degree of proteinuria as an indication for ST in adult IgAN patients. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

This was an open, randomized study of the cardiovascular effects of the histamine H receptor antagonists ranitidine, famotidine, and nizatidine after single oral doses alone or in combination in healthy volunteers. When compared with placebo ranitidine (450 mg) did not have any haemodynamic effects. Nizatidine (300 mg) caused significant falls in heart rate and cardiac output. Famotidine (40 mg) caused significant falls in stroke volume and cardiac output and an increase in pre-ejection period. Pretreatment with ranitidine abolished the haemodynamic effects of nizatidine and caused a time-shift of 2 h in the onset of the cardiovascular effects of famotidine. The difference in the results for nizatidine and famotidine can be explained by the longer half-life of famotidine. Vascular effects are assumed to be responsible for impairment of cardiac performance by famotidine. [ABSTRACT FROM AUTHOR]

The potential for interaction between ibuprofen and two histamine H-receptor blocking drugs - nizatidine and cimetidine - was investigated in six healthy male volunteers aged 20 to 25 years. Each subject received placebo, nizatidine 300 mg and cimetidine 800 mg orally at 9.00 p.m. daily for six doses in three randomised treatment periods separated by eight days. On the third day of each treatment period ibuprofen 400 mg was administered at the same time and venous blood samples were taken at intervals throughout the night and subsequently up to 84 h after administration. There was no difference in the area under the plasma concentration-time curve, rate of absorption or half-life of elimination of ibuprofen between the three treatments. The elimination half-life of ibuprofen on placebo was 2.04 h. The elimination half-life of nizatidine on ibuprofen was 1.72 h and that of cimetidine was 3.54 h. The latter is higher than previously reported in normal subjects. It is concluded that neither H-blocker affects the kinetics of ibuprofen in man. [ABSTRACT FROM AUTHOR]

Background: Peptic ulcer is an excoriated area of stomach or intestinal mucosa. Two experimental designs were proceeded: the first aimed. on twenty adult male albino rats, used to study the protective effect of both ranitidine and nizatidine; on the second, including sixty adult male albino rats, was used to study the therapeutic effect of ranitidine and nizatidine after induction of ulcer and also to evaluate the adverse effects of therapeutic doses of H2-receptor antagonists on male hormonal profile. The study aims to assess the gastroprotective effects of nizatidine and ranitidine and on treating of non-steroidal anti-inflammatory drugs (NSAIDs) induced peptic ulcer and to evaluate its adverse effect on male sex hormones. Result: The result revealed that ranitidine and nizatidine reduced incidence of ulceration. Histopathological findings showed a significant recovery of the alteration, and disturbance in male sex hormones. Conclusion: Nizatidine is better than ranitidine in the management of NSAIDs induced peptic ulcer in rats. [ABSTRACT FROM AUTHOR]

We report on a hemodialysis (HD) patient in whom fatal aplastic anemia developed after the administration of nizatidine, a histamine 2 (H2)-receptor antagonist. The patient was a 55-year old Japanese woman and had been on HD for 2 years due to endstage diabetic nephropathy. The patient had a hemorrhagic duodenal ulcer and had been treated with lansoprazole, a proton pump inhibitor, for 2 months. After improvement, lansoprozole was discontinued and she was subsequently treated with nizatidine. Twelve days after initiation of nizatidine treatment, the patient developed a high-grade fever with symptoms suggestive of upper respiratory infection. Hematological tests showed severe pancytopenia, and drug-induced aplastic anemia was diagnosed. Nizatidine was suggested as the causal drug. Despite intensive therapies, the patient died on the 23rd hospital day from generalized fungal infections. Although hematological adverse events have been reported in HD patients receiving H2-receptor antagonists, few studies of fatal aplastic anemia associated with these drugs have been reported. This case emphasized that careful observation is required after the initiation of H2-receptor antagonist treatment in HD patients. [ABSTRACT FROM AUTHOR]