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At least 19 recordsLinked to original sources
PubMed2004

Influence of antazoline and ketotifen on the anticonvulsant activity of conventional antiepileptics against maximal electroshock in mice.

Experimental studies have indicated that the central histaminergic system plays an important role in the inhibition of seizures through the stimulation of histamine H1 receptors. H1 receptor antagonists, including classical antiallergic drugs, occasionally may induce convulsions in healthy children and patients with epilepsy. The purpose of this study was to investigate the effects of antazoline and ketotifen (two H1 receptor antagonists) on the anticonvulsant activity of antiepileptic drugs against maximal electroshock (MES)-induced convulsions in mice. The following antiepileptic drugs were used: valproate, carbamazepine, diphenylhydantoin and phenobarbital. In addition, the effects of antiepileptic drugs alone or in combination with antazoline or ketotifen were studied on long-term memory (tested in the passive avoidance task) and motor performance (evaluated in the chimney test), acutely and after 7-day treatment with these H1 receptor antagonists. The influence of antazoline and ketotifen on the free plasma and brain levels of the antiepileptics was also evaluated. Antazoline (at 0.5 mg/kg), given acutely and after 7-day treatment, significantly diminished the electroconvulsive threshold. Similarly, ketotifen, after acute and chronic doses of 8 mg/kg markedly reduced the threshold for electroconvulsions. In both cases, antazoline and ketotifen were without effect upon this parameter at lower doses. Antazoline (0.25 mg/kg) significantly raised the ED50 value of carbamazepine against MES (both, acutely and after 7-day treatment). Furthermore antazoline (0.25 mg/kg) also reduced the anticonvulsant activity of diphenylhydantoin, but only after repeated administration, without modifying the brain and free plasma level of this drug. Moreover, valproate and phenobarbital did not change their protective activity when combined with antazoline. Ketotifen (4 mg/kg) possessed a biphasic action, acutely it enhanced the anticonvulsant action of carbamazepine and phenobarbital while, following 7-day treatment, reduced the antiseizure activity of carbamazepine. Ketotifen did not affect the free plasma or brain levels of antiepileptics tested. Only acute antazoline (0.25 mg/kg) applied with valproate impaired the performance of mice evaluated in the chimney test. Ketotifen (4 mg/kg) co-administered with conventional antiepileptic drugs impaired motor coordination in mice treated with valproate, phenobarbital or diphenylhydantoin. Acute and chronic antazoline (0.25 mg/kg) alone or in combination with antiepileptic drugs did not disturb long-term memory, tested in the passive avoidance task. Similarly, ketotifen (4 mg/kg) did not impair long-term memory, acutely and after 7-day treatment. However, valproate alone or in combination with chronic ketotifen (4 mg/kg) worsened long-term memory. The results of this study indicate that H1 receptor antagonists, crossing the blood brain barrier, should be used with caution in epileptic patients. This is because antazoline reduced the protective potential of diphenylhydantoin and carbamazepine. Also, ketotifen reduced the protection offered by carbamazepine and elevated the adverse activity of diphenylhydantoin, phenobarbital and valproate.

Animals↗
PubMed2003

Neuroprotective activity of antazoline against neuronal damage induced by limbic status epilepticus.

Imidazoline drugs exert neuroprotective effects in cerebral ischaemia models. They also have effects against mouse cerebellar and striatal neuronal death induced by N-methyl-D-aspartate (NMDA) through the blockade of NMDA currents. Here, we investigated the effects of antazoline on NMDA toxicity and current in rat hippocampal neuronal cultures, and on an in vivo model of status epilepticus. In hippocampal cultures, antazoline (30 microM) decreased NMDA-mediated neurotoxicity and also blocked the NMDA current with voltage-dependent and fast-reversible action (inhibition by 85+/-3% at -60 mV). Status epilepticus was induced by injecting pilocarpine (200 nmol) directly into the right pyriform cortex of male adult rats. The rats then received immediately three consecutive i.p. injections at 30-min intervals of either PBS (control group) or antazoline at 10 mg/kg (low-dose group) or at 45 mg/kg (high-dose group). During the 6-h recording, status epilepticus lasted more than 200 min in all groups. In the high-dose group only, seizures completely ceased 1 h after the third injection of antazoline, then started again 1 h later. Rats were killed 1 week later, and Cresyl Violet-stained sections of their brain were analysed for damage quantification. On the ipsilateral side to the pilocarpine injection, pyriform cortex and hippocampal CA1 and CA3 areas were significantly protected in both antazoline-treated groups, whilst prepyriform and entorhinal cortices were only in the high-dose group. On the contralateral side to the pilocarpine injection, only the hippocampal CA3 area was significantly protected in the low-dose group, but all investigated structures were in the high-dose group. In conclusion, antazoline is a potent neuroprotective drug in different models of neuronal primary culture, as previously shown in striatal and cerebellar granule neurons [Neuropharmacology 39 (2000) 2244], and here in hippocampal neurons. Antazoline is also neuroprotective in vivo in the intra-pyriform pilocarpine-induced status epilepticus model.

Animals↗
PubMed1997

Antazoline increases insulin secretion and improves glucose tolerance in rats and dogs.

In vivo effects of an imidazoline devoid of alpha2-adrenoceptor antagonistic properties, antazoline, on insulin secretion and glycemia were investigated both in fasted rats and dogs. In both species, antazoline (1.5 mg/kg i.v.) transiently increased insulinemia without affecting basal plasma glucose levels. In contrast, during an i.v. glucose tolerance test, antazoline markedly potentiated insulin release and thus increased the glucose disappearance rate. In rats, during an oral glucose tolerance test, the intragastric administration of antazoline (1.5 mg/kg) clearly enhanced insulin secretion and reduced hyperglycemia. In dogs provided with a venous pancreatico-duodenal bypass, antazoline (0.5 mg/kg i.v.) induced an immediate and transient increase in insulin and somatostatin but not in glucagon pancreatico-duodenal outputs. In conclusion, intravenously and orally administered, the imidazoline antazoline is able to stimulate insulin secretion in vivo and improve glucose tolerance. The imidazoline compounds could therefore have a potential therapeutic relevance as new antihyperglycemic insulinotropic agents.

Animals↗
PubMed2006

A rapid derivative spectrophotometric method for simultaneous determination of naphazoline and antazoline in eye drops.

A zero-crossing first-derivative spectrophotometric method is applied for the simultaneous determination of naphazoline hydrochloride and antazoline phosphate in eye drops. The measurements were carried out at wavelengths of 225 and 252 nm for naphazoline hydrochloride and antazoline phosphate, respectively. The method was found to be linear (r2>0.999) in the range of 0.2-1 microg/ml for naphazoline hydrochloride in the presence of 5 microg/ml antazoline phosphate at 225 nm. The same linear correlation (r2>0.999) was obtained in the range of 1-10 microg/ml of antazoline phosphate in the presence of 0.5 microg/ml of naphazoline hydrochloride at 252 nm. The limit of determination was 0.2 microg/ml and 1 microg/ml for naphazoline hydrochloride and antazoline phosphate, respectively. The method was successfully used for simultaneous analysis of naphazoline hydrochloride and antazoline phosphate in eye drops without any interference from excipients and prior separation before analysis.

Adrenergic alpha-Agonists↗
PubMed1978

Improved spectrophotometric determination of antazoline.

A simple, precise, and accurate spectrophotometric determination of antazoline salts was developed by improving the ceric sulfate procedure. Replacement of water with acetic acid for the preparation of all assay solutions permitted reproducible measurements of the chromogen that absorbed at 505 nm. An appreciable increase in color stability was attained by the controlled addition of perchloric acid to the ceric reagent prior to interaction with antazoline at room temperature. Evidence is provided to account for the oxidation of antazoline at the expense of a complex ceric species. Other 2-imidazolines or phenylephrine did not interfere with the investigated color reaction. In addition to the high value of the chromogen molar absorptivity, ideal adherence of color absorption to Beer's law permitted accurate and reproducible estimation of antazoline over the 1--10-microgram range. The procedure was applied to the analysis of different antazoline dosage forms.

Antazoline↗
PubMed1975

Antazoline therapy of recurrent refractory supraventricular arrhythmias--a preliminary report.

Seven patients with chronic or recurrent supraventricular tachyarrhythmias were selected for a trial of antazoline therapy because sinus rhythm or a controlled ventricular response could not be achieved with quinidine, procainamide, digitalis or propranolol. Sinus rhythm was established by either intravenous administration of antazoline or direct-current countershock, and has been maintained in all for 4 to 16 months by oral administration of antazoline. Side effects were minor. Antazoline is a sufficiently promising antiarrhythmic agent to warrant large-scale controlled studies.

Adolescent↗
PubMed1978

Polarographic estimation of antazoline hydrochloride.

The dc-polarographic investigation of antazoline hydrochloride in aqueous acidic media is described. Using potassium chloride-hydrochloric acid mixture as the supporting electrolyte (pH = 3.25), antazoline hydrochloride was electrochemically reduced at the dropping mercury electrode, with the production of two waves with E1/2 values of --1.35 and --1.65 V respectively. As revealed from the study of the effect of mercury column height, pH of the medium and concentration of the depolarizer, the polarographic reduction of the antazolinium cation is preceded by a catalytic H-wave. The diffusion-controlled nature of the electrode process permitted the quantitative determination of antazoline hydrochloride in concentrations down to 1.0 . 10(-4)M. Application of the presented procedure to the analysis of different dosage forms of the compound studied proved successful and compared favourably with official estimations of anatazoline salts. In view of its simplicity, accuracy and sensitivity, the presented polarographic method can be recommended for routine analysis of antazoline formulations.

Antazoline↗
PubMed1995

Synthesis and identification of the primary degradation product in a commercial ophthalmic formulation using NMR, MS, and a stability-indicating HPLC method for antazoline and naphazoline.

HPLC analysis of an anti-infective ophthalmic solution (Albalon-A), containing the active drugs naphazoline and antazoline, revealed a degradation peak of unknown identity. To elucidate the identity of the degradant, the active drugs were each hydrolyzed by refluxing at high pH, and their respective hydrolysis products were isolated and spectrally characterized by NMR, FT-IR, and MS for conclusive structure elucidation. The degradant's identity was confirmed by HPLC-MS analysis of Albalon-A ophthalmic solution to be the antazoline hydrolysis product N-[(N-benzylanilino)acetyl]ethylenediamine (IV). A stability-indicating HPLC method was then developed which was able to resolve IV from the active drugs. This HPLC method was then validated for quantitating the active drugs and IV. Validation studies demonstrated linear UV response at 280 nm, recovery > 98%, good reproducibility, and a detection limit of 2 micrograms/mL IV. Overall, the data demonstrated that the HPLC method was quantitative and specific for antazoline, naphazoline, and IV. Analysis of an expired stabilitry lot of the ophthalmic solution indicated the concentration of IV was 0.002% (w/v).

Antazoline↗
PubMed1986

Antazoline as an adjuvant in immunosuppressive therapy in renal transplant patients.

The survival of transplanted cadaver kidneys was compared in a group of 33 first-transplant patients treated with antazoline (Antistine) in addition to conventional immunosuppressive therapy (group A) and a group of 36 patients receiving immunosuppressive therapy only (group B). After 1 year, the transplant survival rate was 79% in group A as compared to 56% in group B (P less than 0.05). The difference which was still present after 2 and 5 years could not be attributed to any other factors that might have influenced the survival rate. Antazoline appears above all to diminish the intensity of moderately severe rejection episodes, which often lead to graft loss inducing a chronic type of rejection reaction. However, the frequency of rejection crises during the first 4 months and the percentages of patients without rejection or with primary irreversible rejection crises were practically the same in the two groups. The mechanism of action underlying this potentially important immunosuppressive effect of antazoline is as yet not clarified.

Adjuvants, Immunologic↗
PubMed1975

Antazoline-induced immune hemolytic anemia, hemoglobinuria, and acute renal failure.

A case of repeated antazoline-induced immune hemolytic anemia, thrombocytopenia, hemoglobinuria, and acute renal failure is reported. The first episode of renal failure occurred after an i.v. pyelography causing an anaphylactic shock, and the two later episodes were preceded by allergic reaction to drugs. Antazoline was given among other remedies, but this drug was the only one used for treatment on every occasion. The clinical picture and the immunological tests, including an antazoline-dependent Coombs' test, indicate that the blood disorders might have been caused by a type 2 allergic reaction and renal lesion by a type 3 reaction, at least on the second and third occasions.

Acute Kidney Injury↗
PubMed1981

Immune thrombocytopenia due to antazoline (Antistina).

Antazoline (Antistina)-induced thrombocytopenic purpura occurring on three occasions in a 21-year-old woman is reported. After withdrawal of the drug ther recovered promptly. In vitro investigation demonstrated the presence of an antibody in serum, which in association with antazoline caused complement fixation when added to test platelets. Also platelet agglutinins could be detected in the patient's serum when antazoline was added. The reactions were drug specific and they could still be demonstrated 9 months after the last exposure to the drug.

Adult↗
PubMed1975

Antazoline phosphate and naphazoline hydrochloride, singly and in combination for the treatment of allergic conjunctivitis-a controlled, double-blind clinical trial.

A controlled, double-blind comparison of naphalzoline hydrochloride 0.05%, antazoline phosphate 0.5%, a combination of both components and a placebo was performed on 51 ragweed sensitive patients presenting allergic conjunctivitis. Evaluation of response at various times after instillation of medication for lacrimation, conjunctival inflammation, pruritus, photophobia and pain showed naphazoline hydrochloride, antazoline phosphate and the combination product superior to placebo. The combination product was statistically significantly superior for conjunctival inflammation and photophobia. The need for post-challenge treatment with epinephrine hydrochloride was significantly less in those eyes treated with the combination product. demonstrating prophylactic efficacy.

Adolescent↗
PubMed1986

Simultaneous high-performance liquid chromatographic determination of antazoline phosphate and tetrahydrozoline hydrochloride in ophthalmic solution.

A method for the determination of 2-[(N-phenyl)benzylaminomethyl]-2-imidazoline X H3PO4 (antazoline phosphate) and 2-(1,2,3,4-tetrahydro-1-naphthyl)-2-imidazoline X HCl (tetrahydrozoline hydrochloride) in ophthalmic solution is described. The pharmaceutical preparation is analysed directly by reversed-phase ion-pair high-performance liquid chromatography and the method is very rapid, selective and simple.

Antazoline↗
PubMed2002

Inhibition of voltage-gated Ca2+ channels by antazoline.

We showed recently that imidazolines exert neuroprotection against hypoxia and NMDA toxicity in cerebellar and striatal neuronal cultures, through a voltage-dependent blockade of glutamatergic NMDA receptors. Here, we report that in striatal neuronal cultures from mouse embryos the imidazoline compound, antazoline, inhibits voltage-gated Ca2+ channels by acting at a phencyclidine-like site. This effect was fast, fully reversible, voltage-dependent and predominant on P/Q- and N-type Ca2+ channels. Taken together, these results suggest that imidazolines may elicit neuroprotective effects also by decreasing the release of glutamate through inhibition of presynaptic Ca2+ channels.

Animals↗
PubMed1991

A comparison of aspiration, antazoline sclerotherapy and surgery in the treatment of hydrocele.

Of 98 hydroceles (mean volume 125 ml) in a consecutive series of 92 patients, treated initially by aspiration, 14% (mean volume 70 ml) were cured. The 76 recurring hydroceles (mean volume 146 ml) were then randomised to either antazoline sclerotherapy on an out-patient basis or surgery. Cure rates were 89 and 100%, respectively, at follow-up 6 months later. Operated patients were admitted for a mean duration of 2.5 days. The results indicated that aspiration alone was inadequate, and sclerotherapy is advocated as the first choice of treatment for hydrocele.

Adult↗
PubMedDate not supplied

Simple HPLC determination of benzalkonium chloride in ophthalmic formulations containing antazoline and tetrahydrozoline.

A simple and rapid analytical procedure for routine quantification of n-C12H25 and n-C14H29 benzalkonium chloride (C-12 and C-14 BKC) homologs in ophthalmic formulations containing antazoline HCl and tetrahydrozoline HCl by high-performance liquid chromatography was developed and validated. The ophthalmic solution samples can be directly analyzed by reversed-phase on HiQ-Sil C18 column (4.6 mm x 150 mm, i.d., 5-microm particle size) with acetonitrile-sodium acetate buffer (pH 5.0; 0.2 M) (70:30, v/v) as mobile phase. UV Detection was carried out at 262 nm. The method was linear over the selected concentration and ranged from 0.03 to 0.10 mg/ml (r2 = 0.9999) and from 0.01 to 0.05 mg/ml (r2 = 0.9979) for C-12 and C-14 BKC homologs, respectively. The mean percent recoveries were 100.2 and 102.6 and the percent CV values were 1.3 and 3.5 for C-12 and C-14 BKC homologs, respectively. The results demonstrated the good linearity, accuracy, and precision. The method was applied to determine two commercial ophthalmic formulations, and the percent label amounts of total BKC contents were found to be 99.7 and 103.2.

Antazoline↗