Am J Hosp Pharm. 1994 Sep 15;51(18):2273-6.
Stability of piperacillin sodium-tazobactam sodium and ranitidine hydrochloride in 0.9% sodium chloride injection during simulated Y-site administration.

Choi JS, Burm JP, Jhee SS, Chin A, Ulrich RW, Gill MA.

Department of Clinical Pharmacy, College of Pharmacy, Chosun University, Kwangju, Republic of Korea.

The stability of piperacillin sodium plus tazobactam sodium and ranitidine hydrochloride in 0.9% sodium chloride injection during simulated Y-site administration was studied. Triplicate test solutions of piperacillin 40 mg/mL plus tazobactam 5 mg/mL (as the sodium salts) or piperacillin 80 mg/mL plus tazobactam 10 mg/mL (as the sodium salts) were mixed 1:1 with ranitidine 0.5 and 2.0 mg/mL (as the hydrochloride salt). The solutions were stored at 23 degrees C, and samples were removed at zero, one, two, and four hours for measurement of drug concentration by stability-indicating high-performance liquid chromatography. At the time of sampling and before any dilution, each sample was visually inspected for color and precipitation, and pH was determined. At all sampling times, the concentrations of piperacillin, tazobactam, and ranitidine were > 90% of initial concentrations. There were no substantial changes in pH or color. Tazobactam 5 mg/mL (as the sodium salt) and ranitidine 0.5 and 2 mg/mL (as the hydrochloride salt) in 0.9% sodium chloride injection were stable for up to four hours during simulated Y-site administration. Piperacillin 80 mg/mL plus tazobactam 10 mg/mL (as the sodium salts) and ranitidine 0.5 and 2 mg/mL (as the hydrochloride salt) were stable for up to four hours during simulated Y-site administration.

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J Assoc Physicians India. 1993 Sep;41(9):584, 589.
Ranitidine for the prevention of complications following endoscopic sclerotherapy for esophageal varices.

Kumar A, Mehta SR, Joshi V, Kasthuri AS, Narayanan VA.

Command Hospital (SC) Pune.

Thirty one patients with significant esophageal variceal bleed were allocated alternately to receive endoscopic sclerotherapy along with ranitidine 300 mg daily or endoscopic sclerotherapy alone till eradication of varices. The mean sclerotherapy sessions, time and volume of sclerosant required for obliteration of varices were similar for the two groups. The esophageal varices were eradicated in all the patients except three in sclerotherapy alone group. There was statistically significant reduction in frequency of post sclerotherapy mucosal ulcers (P < 0.05) after addition of ranitidine to sclerotherapy. Rebleeding was not only significantly reduced (P < 0.05) in the sclerotherapy with ranitidine group but was minor and did not even require blood transfusion. In sclerotherapy alone group rebleeding was controlled by surgery in two patients and one died due to massive bleeding. The results of this study suggest a beneficial role of ranitidine in reducing post sclerotherapy mucosal ulcers and rebleeding. This effect of ranitidine emphasises the role of acid-pepsin in pathogenesis of these ulcers and its associated morbidity.

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Xenobiotica. 1993 Nov;23(11):1263-75.
Renal clearance of pyridostigmine in myasthenic patients and volunteers under the influence of ranitidine and pirenzepine.

Eiermann B, Sommer N, Winne D, Schumm F, Maier U, Breyer-Pfaff U.

Institute of Toxicology, University of Tubingen, Germany.

1. To assess the contribution of tubular secretion to the renal excretion of pyridostigmine, and its modification by other cationic drugs, six volunteers were given single oral doses of 60-mg pyridostigmine bromide with and without co-administration of ranitidine or pirenzepine. Renal clearances were determined by h.p.l.c. analysis of pyridostigmine and enzymic measurement of endogenous creatinine in plasma and urine. 2. In patients with myasthenia receiving continuous pyridostigmine therapy, renal clearance values were obtained in the same manner with and without ranitidine (10 patients) or pirenzepine (nine patients) co-medication. 3. Pyridostigmine was not bound to plasma proteins. Its renal clearance averaged 6.65 ml/min per kg (350% of the creatinine clearance) in all subjects, 74% being due to net tubular secretion. 4. Mean values for pyridostigmine renal clearance and for clearance by secretion were decreased in the presence of pirenzepine, but plasma concentrations were not affected significantly. Ranitidine caused a small non-significant decrease of the pyridostigmine clearance in patients. 5. Pyridostigmine had a higher elimination (2 h-1) than the absorption rate constant (0.23 h-1) when administered orally as a non-retarded preparation. 6. The renal clearance of creatinine was slightly increased by pyridostigmine in volunteers and slightly decreased by pirenzepine in the total group of subjects.

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Dig Dis Sci. 1994 Feb;39(2):410-7.
Basal acid output and gastric acid hypersecretion in gastroesophageal reflux disease. Correlation with ranitidine therapy.

Collen MJ, Johnson DA, Sheridan MJ.

Department of Medicine, Loma Linda University Medical Center, California.

The purpose of this study was to evaluate possible differences in basal gastric acid secretion with regard to severity of gastroesophageal reflux disease. Basal acid output was determined by nasogastric suction in 228 patients with gastroesophageal reflux disease who received upper gastrointestinal endoscopy and were diagnosed with either pyrosis alone (N = 98), erosive esophagitis with or without pyrosis (N = 87), or Barrett's esophagus (N = 43). Mean basal acid output for the 228 patients with gastroesophageal reflux disease was 6.5 +/- 5.6 meq/hr, which was significantly different from 65 normal subjects with a mean basal acid output of 3.0 +/- 2.7 meq/hr (P < 0.0001). Compared to normal subjects, mean basal acid outputs significantly differed for patients with pyrosis (P < 0.05), esophagitis (P < 0.01), and Barrett's esophagus (P < 0.01). There was also a significant difference in mean basal acid output between the patients with pyrosis and Barrett's esophagus (P < 0.01). Nineteen of the 98 patients with pyrosis (19%), 24 of the 87 patients with esophagitis (28%), and 15 of the 43 patients with Barrett's esophagus (35%) had gastric acid hypersecretion (basal acid output greater than 10.0 meq/hr). One hundred forty-six patients with gastroesophageal reflux disease were treated with ranitidine in doses that resulted in complete healing of esophagitis and disappearance of pyrosis. Ninety-three patients responded to ranitidine 300 mg/day; however, 53 patients required increased dose of ranitidine (mean 1205 mg/day, range 600-3000 mg/day).(ABSTRACT TRUNCATED AT 250 WORDS)

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Arch Dis Child. 1993 May;68(5 Spec No):602-3.
Ranitidine pharmacokinetics in newborn infants.

Fontana M, Massironi E, Rossi A, Vaglia P, Gancia GP, Tagliabue P, Principi N.

Fourth Department of Paediatrics, University of Milan Medical School, Italy.

Few data are available for ranitidine pharmacokinetics in the first few days of life. Twenty seven newborn infants were treated with intravenous ranitidine because they were vomiting blood, although they had a negative Apt's test. Each infant provided two blood samples at randomly selected times 30-360 minutes after a 2.4 mg/kg intravenous bolus of ranitidine. A single exponential equation for the concentration-time graph was fitted to the mean serum concentrations at different times. From this model the following mean (SD) measurements wer derived: elimination half life, 207.1 (19.1) minutes; total volume of distribution, 1.52 (0.91) l/kg; and total plasma clearance, 5.02 (0.46) ml/kg/min. Assuming that these measurements do not change with different administered doses, regimens can be derived to assist in planning ranitidine treatment in newborn infants.

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J Pharm Sci. 1993 Jun;82(6):601-4.
Effects of temperature and relative humidity on the solid-state chemical stability of ranitidine hydrochloride.

Teraoka R, Otsuka M, Matsuda Y.

Department of Pharmaceutical Technology, Kobe Women's College of Pharmacy, Japan.

The chemical stability of ranitidine HCl in solution and in the solid state at various temperatures was investigated by high-performance liquid chromatography. Ranitidine HCl was unstable in lower pH buffer solutions, and the percent degradation after 72 h increased as the pH of the buffer solution was reduced. The percent degradation in the unbuffered solution increased dose dependently. The critical relative humidity (CRH) of the ranitidine HCl bulk powder was approximately 67% relative humidity (RH). The amount of water adsorbed onto the sample above the CRH was proportional to the RH level. The percent degradation of the powder below 50% RH was almost negligible because, at this level, it was a solid. The percent degradation at 60-70% RH was higher than that above 70% RH. Ranitidine HCl powder was unstable around the CRH.

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Arch Dis Child. 1993 Jul;69(1 Spec No):37-9.
The effect of intravenous ranitidine on the intragastric pH of preterm infants receiving dexamethasone.

Kelly EJ, Chatfield SL, Brownlee KG, Ng PC, Newell SJ, Dear PR, Primrose JN.

St James's University Hospital, Academic Unit of Paediatrics and Child Health, Leeds.

Gastric perforation is a catastrophic, albeit uncommon, side effect of steroid treatment for premature infants with bronchopulmonary dysplasia (BPD). A reduction of intragastric acidity may protect against peptic ulceration. The effect of different doses of ranitidine, given as intravenous infusions, on intragastric acidity in premature neonates was therefore examined. Ten consecutive, enterally starved, infants receiving dexamethasone (0.6 mg/kg) for BPD were enrolled. Intragastric pH was continuously monitored on the day before steroid treatment and on the four following days, initially without H2 blockade and then using a continuous intravenous infusion of ranitidine at 0.031, 0.0625, and 0.125 mg/kg/hour. An infusion of 0.0625 mg/kg/hour of ranitidine was sufficient to increase and maintain gastric pH above 4; the authors therefore use this infusion during dexamethasone administration as possible prevention of gastric perforation.

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Aliment Pharmacol Ther. 1993 Jun;7(3):237-46.
Gastric anti-secretory, mucosal protective, anti-pepsin and anti-Helicobacter properties of ranitidine bismuth citrate.

Stables R, Campbell CJ, Clayton NM, Clitherow JW, Grinham CJ, McColm AA, McLaren A, Trevethick MA.

Glaxo Group Research Ltd, Ware, Herts, UK.

Ranitidine bismuth citrate is a novel compound formed from ranitidine and a bismuth citrate complex. In conscious dogs, ranitidine bismuth citrate had similar activity to ranitidine hydrochloride as an inhibitor of histamine-induced gastric acid secretion when oral doses containing equivalent amounts of ranitidine base (0.1 or 0.3 mg/kg) were compared. In the rat, ranitidine bismuth citrate (3-30 mg/kg p.o.) prevented gastric mucosal damage induced by ethanol (fundic damage) and indomethacin (antral damage). Ranitidine hydrochloride and tripotassium dicitrato bismuthate were also effective against indomethacin-induced damage, but were both significantly less potent than ranitidine bismuth citrate in this model. Ranitidine hydrochloride was inactive against ethanol-induced damage. In vitro, ranitidine bismuth citrate (1 mmol/L) inhibited human pepsin isoenzymes 1, 2, 3 and 5. Pepsin 1 was inhibited to a similar extent by ranitidine bismuth citrate, bismuth citrate and tripotassium dicitrato bismuthate at concentrations equivalent to 1 mmol/L bismuth, but ranitidine (1 mmol/L) was inactive. Ranitidine bismuth citrate was more potent than tripotassium dicitrato bismuthate as an inhibitor of pepsins 2, 3 and 5. Ranitidine bismuth citrate inhibited both Helicobacter pylori (effective concentration 4-32 micrograms bismuth/ml) and H. mustelae (1-4 micrograms bismuth/ml); similar results were obtained with tripotassium dicitrato bismuthate. Bismuth citrate was slightly less effective, and ranitidine hydrochloride was inactive (> 125 micrograms/ml). In ferrets naturally colonized with H. mustelae, oral treatment with ranitidine bismuth citrate, 12 or 24 mg/kg twice daily for 4 weeks, caused a dose re




Am J Vet Res. 1993 Jul;54(7):1103-7.
Effect of ranitidine on healing of experimentally induced gastric ulcers in ponies.

MacAllister CG, Sangiah S.

Department of Medicine and Surgery, College of Veterinary Medicine, Oklahoma State University, Stillwater 74078.

Thirty young ponies were examined endoscopically for evidence of gastric ulceration. Seven ponies had noninduced gastric ulcers present at the initial examination and were eliminated from the study. In an attempt to induce gastric ulcers experimentally, flunixin meglumine (1.1 mg/kg of body weight, IM, q 8 h) was administered for 7 days to the 23 ponies with endoscopically normal gastric mucosa. During the 7 days of flunixin administration, 11 ponies developed gastric ulcers that were appropriate for study. The 11 ponies were randomly allotted to 2 groups. Group-A (n = 5) and group-B (n = 6) ponies received ranitidine (4.4 mg/kg, PO, q 8 h) and corn syrup, respectively, until ulcers healed or for a maximum of 40 days. General anesthesia was induced every 3 to 5 days for visual evaluation of ulcer healing by use of a video endoscope. The earliest complete healing of gastric lesions observed in a corn syrup-treated pony was at 17 days. At 40 days, 3 of 5 and 3 of 6 ponies of the ranitidine and corn syrup-treated groups, respectively, had healed ulcers. Results of this study indicate that: noninduced gastric ulcers may be common in young ponies, flunixin meglumine may be effective in inducing gastric ulcers for gastric healing studies in young ponies, and ranitidine (4.4 mg/kg, q 8 h) is not significantly effective in accelerating healing of experimentally induced gastric ulcers in ponies under conditions of this study.

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