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At least 19 recordsLinked to original sources
PubMed1992

Nizatidine versus placebo in active benign gastric ulcer disease: an eight-week, multicenter, randomized, double-blind comparison. The Nizatidine Benign Gastric Ulcer Disease Study Group.

STUDY OBJECTIVE: To determine if 150 mg nizatidine twice daily or 300 mg nizatidine at bedtime are similarly effective and to compare each dose with placebo in healing benign gastric ulcers and relieving peptic ulcer symptoms. METHODS: This study was a randomized, double-blind, placebo-controlled parallel comparison. The study was conducted at 74 gastroenterology and internal medicine clinics in the United States and Canada. Four hundred fifty-six patients with active benign gastric ulcer documented by endoscopy participated in the study. On the basis of a computer-generated randomization list, patients were assigned sequentially to receive either 150 mg nizatidine twice daily (n = 151), 300 mg nizatidine once daily at bedtime and identically appearing placebo capsules in the morning (n = 153), or placebo capsules twice daily (n = 152). Treatment lasted for 8 weeks unless healing was documented by endoscopy after 4 weeks. Antacid tablets (aluminum hydroxide, magnesium hydroxide, simethicone combination) were supplied for relief of symptoms. MEASUREMENTS AND MAIN RESULTS: Both doses of nizatidine significantly improved healing rates at 8 weeks compared with placebo. Daytime and nighttime symptom severity was improved by both nizatidine regimens at end point (p less than 0.015 versus placebo, two-tailed test). Antacid use was similar for all groups in the end point analysis. Patient well-being was significantly better in patients treated with nizatidine than in patients in the placebo group ((p less than 0.04, two-tailed test). No clinically significant differences in the incidence of adverse clinical or laboratory events were noted. CONCLUSION: Nizatidine, 300 mg at bedtime and 150 mg twice daily, resulted in greater healing of benign gastric ulcers than placebo treatment after 8 weeks. Relief of the symptoms of gastric ulcer was significantly better in the patients receiving nizatidine treatment versus placebo treatment.

Capsules↗
PubMed1993

Twenty-four-hour control of gastric acidity by twice-daily doses of placebo, nizatidine 150 mg, nizatidine 300 mg, and ranitidine 300 mg.

This study was carried out to assess the effects on gastric acidity of placebo twice daily (bid), nizatidine 150 mg bid, nizatidine 300 mg bid, and ranitidine 300 mg bid by means of continuous 24-hour intragastric pH monitoring. Twelve patients with duodenal ulcer in remission were randomized to receive in single-blind fashion the above medications on four separate occasions, at least 1 week apart. The three active regimens produced higher pH values (P < .001) and maintained gastric pH above 3.0 units for a longer period (P < .001) than placebo in all time intervals but evening. Nizatidine 150 mg bid caused a lower rise in pH than nizatidine 300 mg bid (P < .01) and ranitidine 300 mg bid (P < .05) during both the daytime and the whole 24 hours. In these time windows also the time spent above 3.0 pH units was significantly shorter for the former regimen than for 300 mg bid of both nizatidine (P < .01) and ranitidine (P < .05). There was no difference between the latter two dosing schedules in terms of both potency and duration of action in all the time intervals considered. It is concluded that twice daily doses of H2 blockers are more effective than placebo in reducing gastric acidity. Three hundred milligrams twice daily of both nizatidine and ranitidine produce a significantly greater and longer-lasting acid suppression than 150 mg bid of nizatidine. Our study also confirms the greater effectiveness of H2 antagonists during nighttime than during day-time.

Adult↗
PubMed1992

Nizatidine versus placebo in gastroesophageal reflux disease. A six-week, multicenter, randomized, double-blind comparison. Nizatidine Gastroesophageal Reflux Disease Study Group.

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.

Double-Blind Method↗
PubMed2000

The effect of previous administration of nizatidine on the neuromuscular effects of vecuronium and the effect of nizatidine on gastric secretion.

Nizatidine, a new H2-receptor antagonist, has been reported to inhibit acetylcholinesterase activity. This could lead to an interaction with neuromuscular blocking drugs. This study examined the effects of nizatidine on the actions of vecuronium. Oral nizatidine has been reported to be an effective protective agent against acid aspiration syndrome, and we reevaluated this effect. The control group (n = 10) received a placebo with water 50 ml and the nizatidine group (n = 10) received nizatidine 300 mg with water 50 ml two hours before arrival in the operating room. Gastric contents were aspirated and the volume and pH measured before induction of anaesthesia. Anaesthesia was induced in all patients with thiopentone 5 mg/kg and 1.5% isoflurane in 98.5% oxygen followed by vecuronium 0.1 mg/kg. Vecuronium onset time and duration time 25 (time from injection until recovery of 25% of vaseline twitch amplitude) were obtained using electromyography. There were no significant differences between the two groups in vecuronium onset time or duration time 25. Gastric fluid volume was greater and gastric pH was lower in the control group than in the nizatidine group. 70% of the control group and none of the nizatidine group (P < 0.005) had a gastric content pH < 2.5 or volume > 25 ml.

Elective Surgical Procedures↗
PubMed1994

Nizatidine versus placebo in gastro-oesophageal reflux disease: a 6-week, multicentre, randomised, double-blind comparison. Nizatidine Gastroesophageal Reflux Disease Study Group.

In a randomised, multicentre trial, nizatidine 150 mg or 300 mg or placebo was administered twice daily for 6 weeks to 515 patients with gastro-oesophageal reflux disease (GORD). Antacid tablets were taken as needed for pain. Significantly superior rates of endoscopically proven complete healing (normal-appearing mucosa) versus placebo occurred after 3 weeks with nizatidine 150 mg and after 6 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 1 day of therapy versus placebo. Twice-daily administration of nizatidine 150 mg or 300 mg provides prompt relief from the major symptom of GORD, heartburn, and complete healing of oesophagitis is seen in many patients.

Adult↗
PubMed1989

Comparison of nizatidine and cimetidine as once-nightly treatment of acute duodenal ulcer. Nizatidine Multicenter Duodenal Ulcer Study Group.

Nizatidine, a new H2-receptor antagonist for the treatment of duodenal ulcer disease, was compared with cimetidine in an 8-wk, randomized, double-blind, multicenter clinical trial. Patients were randomly allocated to receive either nizatidine 300 mg h.s. or cimetidine 800 mg h.s. Patients were treated for 8 wk, regardless of the healing status of their ulcers. An endoscopy was performed at Wk 2, 4, and 8. Healing rates with nizatidine 300 mg h.s. were numerically, but not statistically significantly, superior to those with cimetidine 800 mg h.s. at each treatment period. Ulcer healing rates at Wk 2, 4, and 8 were 41% (78/191), 73% (130/179), and 81% (145/179) for nizatidine and 33% (60/184), 67% (116/174), and 75% (126/168) for cimetidine, respectively. Symptoms of peptic ulcer disease were similarly reduced at each treatment period by nizatidine and cimetidine. Patients with healed ulcers at either Wk 2 or Wk 4 were continued on therapy and an endoscopy was performed at Wk 8. Ulcer recurrence occurred in 10% of nizatidine-treated and 19% of cimetidine-treated patients at Wk 8 (p = 0.085). The observation of recurrence of duodenal ulcer while patients were receiving full-dose H2-receptor antagonist therapy has not been reported previously.

Acute Disease↗
PubMed1989

[Treatment of acute stomach ulcer with H2 receptor antagonists. A direct therapy comparison with 300 mg nizatidine nightly and 2 times 150 mg nizatidine with twice daily 150 mg ranitidine].

In this endoscopically controlled, double-blind study involving 242 patients with acute benign gastric ulcer, it was shown that the selective inhibition of nocturnal gastric acid secretion with 300 mg nizatidine administered on retiring represents an effective and reliable form of therapy. After four weeks of treatment, 90% of the patients receiving 300 mg nizatidine, no longer experienced nocturnal pain, in comparison with 83% receiving 2 X 150 mg nizatidine daily (n.s.). The total healing rates after four weeks were 60% in the patients receiving 300 mg nizatidine, 60% in those on 2 X 150 mg nizatidine daily, and 58% in those receiving 2 X 150 mg ranitidine daily. After eight weeks, the respective figures rose to 85%, 84% and 84%. Clinically relevant side effects were observed in none of the three groups. With a dose on retiring of 300 mg nizatidine, it is possible to accelerate the healing of a benign gastric ulcer, simply by the nocturnal suppression of gastric acid production, and, during the day, preserving physiological gastric function, thus avoiding the possible risks of protracted hypochlorhydria.

Adolescent↗
PubMed1994

Continuous infusions of nizatidine are safe and effective in the treatment of intensive care unit patients at risk for stress gastritis. The Nizatidine Intensive Care Unit Study Group.

This multicentre, randomized, parallel, double-blind study compared the safety and efficacy of nizatidine 20 and 10 mg/h with placebo. The objective was to maintain gastric pH > 4 in seriously ill patients at risk for stress gastritis. Gastric aspirate was obtained at 2-h intervals through a nasogastric tube after beginning study drug, and tested for pH and the presence of blood. Antacid doses (15 ml per dose) were individually adjusted and administered whenever the gastric pH was < 4. Significant gastrointestinal bleeding was assessed clinically by Hemmocult results, presence of frank bleeding from the GI tract, number of transfusions and vital signs. One hundred and twenty-six patients, 43 nizatidine 20 mg/h, 43 nizatidine 10 mg/h and 40 placebo were admitted to the study. For the treatment period, patients treated with either dose of nizatidine required significantly less antacid than placebo treated patients to maintain gastric acid pH > or = 4 (median total: 45 ml versus 180 ml, p < 0.001). Adverse clinical and laboratory events were similar or less frequent in the nizatidine groups compared with placebo. Nosocomial pneumonia occurred with very low frequency in all treatment groups.

Adult↗
PubMed1989

[Nizatidine versus ranitidine in the treatment of acute duodenal ulcer. Comparison of 300 mg nizatidine and 300 mg ranitidine in a single evening dose].

In a double-blind, endoscopically controlled study on 367 duodenal ulcer patients, we compared the clinical efficacy of 300 mg ranitidine nocte with that of 300 mg nizatidine nocte, which is known to reliably provide selective inhibition of nocturnal acid secretion. Nizatidine was administered to 183, ranitidine to 184 patients. Endoscopy was performed at the start of the study, as well as at 2, 4 and 8 weeks. The presence of ulcer was defined as a benign lesion of the gastric mucosa measuring at least 5 mm in diameter; healing was characterized as complete reepithelialization. In the nizatidine group, as many as 76% of our patients were free from night pain at 2 weeks, and 88% at 4 weeks. Identical values were obtained in the group treated with 300 mg ranitidine nocte. The healing rates at 2, 4 and 8 weeks were comparable in the nizatidine and ranitidine groups (nizatidine: 57%, 87%, 92%, respectively; ranitidine: 63%, 90%, 96%, respectively). Clinically significant adverse effects were seen in neither of the two treatment groups. These results demonstrate that selective inhibition of nocturnal acid secretion achieves healing of duodenal ulcer and freedom from pain as rapidly and effectively as protracted inhibition of acid secretion provided by the administration of 300 mg ranitidine nocte.

Adolescent↗
PubMed1988

Twenty four hour intragastric acidity and plasma gastrin concentration in healthy volunteers taking nizatidine 150 mg, nizatidine 300 mg, ranitidine 300 mg, or placebo at 21:00 h.

Nine healthy volunteers were studied on the seventh day of dosing at 21:00 h with nizatidine 150 mg (N 150), nizatidine 300 mg (N 300), ranitidine 300 mg (R 300), or placebo, given in a predetermined random order. The double-blind 24 hour studies, using the Royal Free Hospital standard protocol, simultaneously measured intragastric acidity and plasma gastrin concentration. Compared with placebo, subjects responded to dosing with each H2-antagonist by a significant decrease of 24 hour intragastric acidity (N 150-45%; N 300-49% R 300-56%; p less than 0.01) and a significant rise of plasma gastrin concentration (N 150 + 20%; N 300 + 27%; R 300 + 58%; p less than 0.01). All three drug regimens caused similar significant decreases of nocturnal acidity (N 150-72%; N 300-79%; R 300-85%; p less than 0.01) and increases of nocturnal plasma gastrin concentration (N 150 + 41%; N300 + 52%; R 300 + 80%; p less than 0.01). Dosing with ranitidine 300 mg at 21:00 h also caused a simultaneous significant decrease of morning acidity (-32%; p less than 0.05) with a significant increase of plasma gastrin concentration (+36%; p less than 0.05), but the antisecretory effects of nizatidine 150 or 300 mg at 21:00 h were only observed during the night, with no effect during the morning. No drug regimen had any effect on acidity or plasma gastrin in the afternoon or early evening.

Adult↗
PubMed1994

Effects of oral nizatidine on preoperative gastric fluid pH and volume in children.

We have studied the effect of oral nizatidine 6 mg kg-1 in total on preoperative gastric fluid pH and volume in children. One hundred and four healthy children, aged 4-11 yr, were allocated randomly to four groups (n = 26): placebo administered at 21:00 and 06:30 the night before and on the day of surgery, respectively (placebo-placebo: control); nizatidine 6 mg kg-1 at 21:00 and placebo at 06:30 (nizatidine-placebo); placebo at 21:00 and nizatidine 6 mg kg-1 at 06:30 (placebo-nizatidine); and nizatidine 3 mg kg-1 at 21:00 and 06:30 (nizatidine-nizatidine). Each child ingested a large volume of apple juice 3 h before estimated induction of anaesthesia. After induction of anaesthesia, pH and volume of gastric fluid obtained via an orogastric tube were measured. Mean pH in the placebo-nizatidine and nizatidine-nizatidine groups was significantly higher than that in the placebo-placebo group (5.7 (SEM 0.3), 6.0 (0.3) vs 1.8 (0.2), respectively) (P < 0.05). Mean pH in the nizatidine-placebo group was similar to that in the control group (2.3 (0.3) vs 1.8 (0.2)). The number of children with pH < 2.5 and volume > 0.4 ml kg-1 in the nizatidine-nizatidine (0%) and placebo-nizatidine (4%) groups was reduced compared with the control (46%) or nizatidine-placebo (38%) group.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed2003

Pharmacokinetics and pharmacodynamics of a novel nizatidine controlled-release formulation in healthy subjects.

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 Cmax by approximately 42% compared to nizatidine IR while maintaining 90% relative bioavailability; tmax 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 AUC 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 AUC 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, thus providing support for the potential utility of nizatidine CR 300 mg dosed at night in alleviating nocturnal symptoms of gastroesophageal reflux disease.

Adolescent↗
PubMed2004

Clinical study on the effects of nizatidine on gastric motility and cardiac autonomic function. Investigations using electrogastrography and spectral analysis of heart rate variability.

Nizatidine (CAS 76963-41-2, Acinon), an H2 receptor antagonist, not only inhibits acid secretion but also improves gastrointestinal motility. However, autonomic nervous function has not been studied in detail using electrogastrography (EGG). In the present study, two protocols were adopted to study nizatidine's effects on cardiac autonomic function and gastric motility. Protocol I--Acute: "Group C-I": 10 healthy volunteers received a single oral dose of nizatidine 150 mg. Protocol II--Chronic: "Group DM without N": 15 patients with diabetes mellitus (DM) were observed prior to administration of nizatidine. "Group DM with N": The same 15 patients with DM received nizatidine 300 mg/day for more than 30 days. "Group C-II": This control group was composed of 15 healthy volunteers not receiving nizatidine. In all groups, EGGs were recorded before and after a meal, and autonomic nervous function and QT interval of ECG dispersions were simultaneously evaluated. In Group C-I, nizatidine significantly increased the peak power amplitude of 3 cycles/min (cpm) frequency, but did not significantly change the dominant frequency of the 3-cpm waves. In Group DM with N, nizatidine administration significantly increased the peak power amplitude from 2.4 cpm or a lower frequency (bradygastria) to 3 cpm. Prior to nizatidine administration but after eating a meal, the peak power amplitude on EGG was not increased in Group DM without N. In Group DM with N, however, the EGG peak power amplitude increased to levels similar to those of the healthy subjects (Group C-II). Neither the single nor the chronic administration of nizatidine significantly prolonged the QT interval or increased the QT dispersion. A spectral analysis of heart rate variability showed that nizatidine administration, whether acute or chronic, did not significantly change the indices of autonomic nervous activity. Nizatidine may promote gastric emptying by inhibiting acetylcholine esterase, thus increasing cholinergic activity, and by acting directly on gastric smooth muscle. The results indicate that because nizatidine increases gastric motility without exerting a negative influence on the autonomic nerves, it may be a useful drug in patients with diabetic neuropathy.

Anti-Ulcer Agents↗
PubMed1985

Intravenous nizatidine kinetics and acid suppression.

The effectiveness of intravenous nizatidine in suppressing gastric acid secretion was evaluated by different methods of inducing secretion in two single-blind studies. In study 1, seven subjects were given single, 20-min intravenous infusions of nizatidine (6.25, 25, 75, 150, or 250 mg) before modified sham feeding (MSF). Gastric acid suppression after nizatidine was contrasted with that after placebo and MSF. All doses of nizatidine reduced secretion; the 150- and 250-mg doses of nizatidine suppressed secretion for at least 2.5 hr. In study 2, eight subjects received one 5-min intravenous infusion of placebo, cimetidine (300 mg), or nizatidine (25, 50, 100, or 250 mg) weekly for 6 wk. Secretion was induced by infusing pentagastrin (2 micrograms/kg/hr) 45 min before the study drug was dosed and for 3.5 hr thereafter. Again, all doses of nizatidine reduced gastric acid, chiefly by decreasing volume. Nizatidine induced a clear dose-response effect; nizatidine (100 mg) and cimetidine (300 mg) had approximately equal suppressive effects. Nizatidine (100 mg) and cimetidine (300 mg) reduced acid output by 62% and 63% and reduced volume of secretion by 48% and 51% over the 3.5-hr period. Gastric acid suppression and plasma nizatidine concentrations were directly related. Nizatidine kinetics were linear and proportional to dose. The t1/2 was 1.3 hr (range 0.7 to 2.1 hr), the volume of distribution was 1.2 +/- 0.5 l/kg, and clearance was 0.6 +/- 0.2 l/kg/hr. Laboratory abnormalities and side effects were minor in both studies.

Adult↗
PubMed2002

Effect of nizatidine on paracetamol and its metabolites in human plasma.

The effect of the histamine H2-receptor antagonist, nizatidine, on plasma concentrations of paracetamol has been investigated with respectto hepatic metabolism. Paracetamol (1000 mg) together with 300 or 150 mg nizatidine or placebo was orally administered to five healthy male volunteers. Venous blood samples were taken before and after administration. Plasma paracetamol and paracetamol conjugates (glucuronide and sulfate) were measured by high-performance liquid chromatography. The pharmacokinetic parameters were calculated from the plasma paracetamol concentration-time curves of each volunteer. The plasma nizatidine concentration was highest (2420.0+/-192.4 and 996.0+/-54.6 ng mL(-1)) in the sample taken 1 h after administration of 300 mg nizatidine (high dose) and 150mg nizatidine (low dose), respectively. Plasma paracetamol concentrations with nizatidine (high and low doses) were increased significantly at 45-120 min and 45-60 min, respectively, compared with placebo. The total area under the plasma paracetamol concentration-time curve from 0 to 180 min (2361.5+/-146.4 and 2085.75+/-73.5 microg min mL(-1)) significantly increased after coadministration of nizatidine (high and low doses), respectively (P < 0.01 vs placebo). Paracetamol glucuronide concentrations with nizatidine (high and low doses) were decreased significantly at 30-45 min and 30 min, respectively, compared with placebo. However, plasma paracetamol sulfate concentrations with nizatidine (high and low doses) were not significantly altered. The coadministration of nizatidine (150 and 300 mg) dose-dependently reduces plasma paracetamol glucuronide concentrations and increases plasma paracetamol concentrations. The effects of nizatidine could result from the inhibition of glucuronyltransferase. Thus, care is necessary when paracetamol and nizatidine are coadministered.

Acetaminophen↗
PubMedDate not supplied

Nizatidine, an H2-blocker. Its metabolism and disposition in man.

The disposition of a single oral dose of about 150 mg of nizatidine, an H2-blocker, was studied in five men. Plasma levels of both parent drug and radioactivity peaked in 1-3 hr. Nizatidine accounted for about 60% of the plasma radioactivity. The t1/2 of nizatidine was 1.6 hr. About 35% of nizatidine became bound to plasma proteins in vitro, particularly to alpha-1-glycoprotein. Warfarin, acetaminophen, phenobarbital, propantheline, diazepam, and propranolol did not notably affect the amount of nizatidine bound. Two to 3 times more radioactivity was in plasma than in blood cells or saliva. Greater than 90% of the dose of nizatidine was excreted in urine, probably by glomerular filtration and active tubular secretion. Nizatidine accounted for about 65% of the urinary radioactivity. The major metabolite of nizatidine was N2-monodesmethylnizatidine; it represented about 7% of the nizatidine dosage. Another metabolite, constituting about 5% of the dose, is proposed to be nizatidine N2-oxide. Nizatidine sulfoxide also may be a minor metabolite of nizatidine.

Adult↗
PubMed1990

Endocrine effects of a new histamine H2-receptor antagonist, nizatidine (LY139037), in the male rat.

A new orally active histamine H2-receptor antagonist, nizatidine (LY139037), was evaluated in male rats for effects on mechanisms regulating accessory sex organ growth and function. Cimetidine antagonized androgen binding to cytosolic receptors in vitro while nizatidine had no effect. Nizatidine and cimetidine were administered at the ED50, 5 X ED50, or 10 X ED50 doses for inhibition of gastric acid secretion previously determined using in vivo dog and rat models. The relative potencies of both agents to antagonize histamine H2-receptor-mediated gastric acid secretory responses have been confirmed in human clinical trials. Neither nizatidine nor cimetidine antagonized the in vivo uptake or nuclear translocation of radiolabeled androgen into the hypothalamic-preoptic-amygdala, pituitary, or ventral prostate. Nizatidine, given at doses equal to and 10 X the ED50 gastric acid secretion inhibitory values, and cimetidine (10 X ED50 value) had no effect on the response of male accessory sex organs to a submaximally stimulating dose of androgen in castrated rats. High doses of dietary nizatidine (greater than 500 mg/kg-day) administered for 6 months did not alter intact rat male accessory sex organ weights or circulating androgen levels relative to untreated controls. Acute administration of either nizatidine or cimetidine produced transient elevations in plasma prolactin (PRL) levels. Cimetidine was more potent and consistent than nizatidine in producing these increases in circulating PRL. The data described herein support the contention that unlike cimetidine, nizatidine is not a pharmacological antagonist of androgen action and has less of a stimulatory effect upon plasma prolactin. Taken together, these studies indicate that in the male rat, nizatidine exhibits a large therapeutic index between its gastric antisecretory activity and potential endocrinological effects.

Androgens↗