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At least 163 records · Page 9Linked to original sources
PubMed1991

Effects of anti-vertigo drugs on medial vestibular nucleus neurons activated by horizontal rotation.

The effects of anti-vertigo drugs on medial vestibular nucleus (MVN) neurons were examined to assess the site and mode of action using cats anesthetized with alpha-chloralose. Single neuron activity in the MVN was extracellularly recorded using a silver wire microelectrode attached along a seven-barreled micropipette, each of which was filled with diphenhydramine, diphenidol, betahistine, glutamate or NaCl. Type I of the MVN neurons were identified according to the responses obtained when the animal placed on a turn-table was rotated sinusoidally. The effects of the drugs were examined on type I neurons which received impulses primarily from the labyrinth and sent them to the oculomotor nuclei. The microiontophoretic application of diphenhydramine, diphenidol and betahistine inhibited rotation-induced firing of type I MVN neurons. Diphenhydramine and diphenidol were more potent than betahistine. These results suggest that these drugs directly act on MVN neurons to reduce the responsiveness to rotatory stimulation.

Animals↗
PubMed1993

Dimaprit, a histamine H2-agonist, inhibits anaphylactic histamine release from mast cells and the decreased release is restored by thioperamide (H3-antagonist), but not by cimetidine (H2-antagonist).

Whether anaphylactic histamine release from rat peritoneal mast cells is influenced by betahistine, a histamine H1-receptor agonist/H3-antagonist, and dimaprit, an H2-agonist, was examined. Treatment with dimaprit at 6 and 60 microM for 20 min significantly inhibited the anaphylactic histamine release, whereas betahistine at up to 80 microM under the same conditions did not affect it. Treatment with dimaprit at 6 and 60 microM for 1 to 20 min and for 5 to 20 min, respectively, caused a time-dependent inhibition of the release, but up to 30 min treatment with 8 and 80 microM betahistine had no effect. The decreased histamine release induced by dimaprit was recovered by neither mepyramine nor cimetidine. However, thioperamide, an H3-selective antagonist, dose-dependently restored the diminished release. From these results, the inhibition of anaphylactic histamine release by dimaprit is not produced by the stimulation of H2-receptors, but involves the stimulation of H3-like receptors or H3-subtype receptors, which are distinct from the H3-receptors located in brain, and suggests that the receptor plays an important role in the negative feedback regulation of histamine release.

Anaphylaxis↗
PubMed1991

Histamine in the treatment of vertigo.

The vasodilating properties of histamine were the basis for histamine treatment of episodic vertigo and other inner ear dysfunctions. The successes obtained led to the development of betahistine: an orally active histamine analogue; its general pharmacology resembles that of histamine. Animal pharmacology experiments proved that betahistine increases cerebral blood flow and probably also affects vestibular neurons. From clinical studies, it appears that betahistine is an effective agent for the symptomatic treatment of Meniere's syndrome. Efficacy has also been shown in the treatment of patients suffering from paroxysmal vertigo.

Animals↗
PubMed1992

Histamine increases cytosolic Ca2+ in dibutyryl-cAMP-differentiated HL-60 cells via H1 receptors and is an incomplete secretagogue.

Human neutrophils and dibutyryl-cAMP (Bt2cAMP)-differentiated HL-60 cells possess receptors for the chemotactic peptide N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMet-Leu-Phe), which mediate activation of phospholipase C, with subsequent increase in cytosolic Ca2+ concentration ([Ca2+]i) and activation of specific cell functions. In many cell types, histamine, via H1 receptors, activates phospholipase C, but it is unknown whether neutrophilic cells possess functional H1 receptors. We compared the effects of histamine with those of fMet-Leu-Phe on activation of these cells. In Bt2cAMP-differentiated HL-60 cells, substances increased [Ca2+]i in the effectiveness order fMet-Leu-Phe greater than histamine greater than betahistine. Pertussis toxin diminished fMet-Leu-Phe-induced rises in [Ca2+]i to a greater extent than those induced by histamine. H1 but not H2 antagonists inhibited histamine- and betahistine-induced rises in [Ca2+]i. fMet-Leu-Phe and histamine activated phospholipase C and increased [Ca2+]i through release of Ca2+ from intracellular stores and sustained influx of Ca2+ from the extracellular space. The substances also induced Mn2+ influx. Ca2+ and Mn2+ influxes were inhibited by 1-(beta-[3-(4-methoxyphenyl)propoxyl]-4-methoxyphenethyl)-1H-imida zole hydrochloride (SK&F 96365). The stimulatory effects of histamine on [Ca2+]i were more sensitive to inhibition by 4 beta-phorbol 12-myristate 13-acetate than were those of fMet-Leu-Phe. Unlike fMet-Leu-Phe, histamine did not activate superoxide anion formation, release of beta-glucuronidase, and tyrosine phosphorylation. In neutrophils, histamine and betahistine did not induce rises in [Ca2+]i. Our data show that (i) in Bt2cAMP-differentiated HL-60 cells, histamine increases [Ca2+]i via H1 receptors coupled to pertussis toxin-sensitive and possibly, pertussis toxin-insensitive heterotrimeric regulatory guanine nucleotide-binding proteins, (ii) histamine activates nonselective cation channels, and (iii) unlike fMet-Leu-Phe, histamine is an incomplete secretagogue.

Betahistine↗
PubMed1989

[The effects of ligustrazine, aspirin and beta-histine on platelet aggregation in patients with acute ischemic stroke].

With a auto-balanced terbidimeter, the effects of ligustrazine, aspirin and betahistine on platelet aggregation were studied in 45 patients with acute ischemic stroke. The adopted parameters were: 1) the maximal aggregation (Amax), 2) the maximal aggregation velocity (Vmax), 3) the effective disaggregation rate in 5 minutes (DA 5), 4) the inhibition rate of aggregation given by drugs (IR), and 5) the concentration causing 50% inhibition of aggregation (IC 50). The results indicated that these three drugs could inhibit platelet aggregation both in vivo and in vitro. Aspirin could promote the aggregated platelets disaggregation in vivo and ligustrazine, in vitro. Regarding the effects on inhibiting platelet aggregation in vitro, ligustrazine was the most noticeable among the 3 drugs and aspirin was more effective than betahistine. The IC50 of ligustrazine, aspirin and betahistine were 0.568 mg/ml, 1,286 mg/ml and 1.722 mg/ml respectively. The authors considered that all three drugs possessed anti-platelet effects but they showed some differences among them.

Aged↗
PubMed1975

Control of the microcirculation of the inner ear.

In general, many similarities are seen between cerebral blood flow and cochlear blood flow in response to vasodilating drugs. Cochlear vessels appear to be weakly controlled by the adrenergic nervous system. Cholinergic agents dilate cochlear vessels, although the vasodilation in the cochlea does not necessarily cause an increase in cochlear blood flow because of the associated hypotension. The effect on the systemic circulation is too profound to make these agents clinically useful. Papaverine, dipyridamole, amyl nitrite, and the plasma kinins produce transient increases in cochlear blood flow. Ten per cent carbon dioxide and 90 per cent oxygen product progressive vasodilation as long as the mixture is inhaled. Hydralazine produces too profound an effect on systemic blood pressure. Histamine and betahistine increase cochlear blood flow but only in doses that produce bronchiospasm in the guinea pig. Nicotinic acid and nicotinyl tartrate have no effect on cochlear blood flow. If one considers safety and efficacy as well as patient tolerance, papaverine appears to be the drug of choice for increasing cochlear blood flow clinically. Histamine and betahistine appear to be acceptable alternatives. Betahistine is no longer available for clinical use because of the failure to demonstrate clinical efficacy of therapy.

Cochlea↗
PubMed1987

Comparison of the effects of histamine H1- and H2-receptor agonists on large and small airways in normal and asthmatic subjects.

It is accepted that histamine H1-receptors are present on human bronchial smooth muscle and that they mediate bronchoconstriction. However, the role of the histamine H2-receptor in the airways of man is less certain. In ten non-asthmatic and five asthmatic subjects we have compared the effects of inhalation of a specific H1-receptor agonist, betahistine, a specific H2-receptor agonist, impromidine and the combined H1- and H2-receptor agonist, histamine, on specific airways conductance and measurements from partial expiratory flow-volume curves. Both histamine and betahistine induced reproducible dose-dependent bronchoconstriction in all subjects, as assessed by all measurements made. Impromidine had no effect on measurements of airways function in either group of subjects. These results confirm the presence of bronchoconstricting H1-receptors, and the absence of significant numbers of H2-receptors on human bronchial smooth muscle. There is no difference in the distribution of these receptors in normal and asthmatic subjects.

Adult↗
PubMed1987

Histamine receptors and pulmonary epithelial permeability.

In seven normal subjects and five asthmatics we have compared the effects of inhaled histamine with that of betahistine (a relatively selective H1-receptor agonist) and that of impromidine (a relatively H2-receptor agonist) on pulmonary epithelial permeability, as measured by the half-time clearance from lung to blood of inhaled 99mTc-DTPA (t1/2LB). Both histamine and betahistine produced statistically significant falls in baseline t1/2LB and peak expiratory flow rate, while impromidine produced no significant effects on either parameter. Similar results were obtained in normal subjects and asthmatics alike. In four of the normal subjects, histamine-induced falls in t1/2LB and peak expiratory flow rate were prevented by oral pretreatment with terfenadine 120 mg but not by cimetidine 400 mg. Histamine-induced increases in lung permeability and bronchoconstriction are both mediated via H1-receptors in normal and asthmatic subjects.

Adult↗
PubMed1988

Clinical evaluation of medical treatment for Menière's disease, using a double-blind controlled study.

There are great variations in the clinical evaluations of the effectiveness of antivertiginous drugs for Meniere's disease. In our clinical evaluation, subjective and objective signs and symptoms of 128 patients with Meniere's disease and of 98 with other peripheral vestibular disorders were analyzed in a double-blind controlled study comparing adenosine triphosphate (ATP) (300 mg) and betahistine (36 mg) each given daily for 4 weeks. The method of administration was the matched-pair-group-method for this double-blind controlled trial. The attending physicians concluded that ATP was significantly more effective than betahistine in the treatment of Meniere's disease and other peripheral vestibular disorders.

Adenosine Triphosphate↗
PubMed1978

[The therapy of tinnitus resulting from blast injury (author's transl)].

In a prospective study aimed at the cure of tinnitus due to blast injury, oral treatment of 172 patients with the mono-substances Betahistine, Pentoxifyllin and Xantinol-nicotinate were compared with those of control patients who received no medications. Patients treated with Pentoxifyllin and Xantinol-nicotinate improved better than the comparative group without therapy although the differences were not considerable. Betahistine as compared with the other groups produced significantly better therapeutic results.

Adolescent↗
PubMed1989

Histamine inhibits activation of human neutrophils and HL-60 leukemic cells via H2-receptors.

The effects of prostaglandin E1 (PGE1) and histamine on activation of superoxide (O2-) formation, exocytosis of beta-glucuronidase and aggregation in human neutrophils and HL-60 leukemic cells were studied. PGE1, histamine and impromidine, a potent H2-agonist, inhibited O2- formation in neutrophils induced by the chemotactic peptide, N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMet-Leu-Phe) with IC50 values of 0.5 microM, 8 microM and 2 microM, respectively. The full H1-agonist and weak partial H2-agonist, betahistine, was much less potent and effective than histamine. Dibutyryl cyclic AMP and forskolin mimicked the effects of histamine and PGE1 on O2- formation. The H2-antagonist, famotidine, competitively reversed histamine-induced inhibition of O2- formation with a pA2 value of 7.5. Histamine inhibited O2- formation when added prior to or after fMet-Leu-Phe. fMet-Leu-Phe-induced aggregation and release of beta-glucuronidase in neutrophils were less sensitive to inhibition by PGE1, histamine, dibutyryl cyclic AMP and forskolin than O2- formation. The inhibitor of cyclic AMP-specific phosphodiesterase, rac-4-(3-butoxy-4-methoxybenzyl)-2-imidazolidinone (Ro 20-1724), additively enhanced the inhibitory effects of histamine and PGE1 on the above cell functions. In HL-60 cells differentiated by dimethyl sulfoxide or dibutyryl cyclic AMP, histamine, impromidine and PGE1 but not betahistine inhibited fMet-Leu-Phe-induced O2- formation as well. Our data suggest that histamine inhibits activation of neutrophils and HL-60 cells via H2-receptors through activation of adenylyl cyclase and increased formation of cyclic AMP.(ABSTRACT TRUNCATED AT 250 WORDS)

4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone↗
PubMed2006

'Complementary ENT': a systematic review of commonly used supplements.

OBJECTIVE: To assess the evidence surrounding the use of certain complementary supplements in otolaryngology. We specifically focussed on four commonly used supplements: spirulina, Ginkgo biloba, Vertigoheel and nutritional supplements (cod liver oil, multivitamins and pineapple enzyme). MATERIALS AND METHODS: A systematic review of the English and foreign language literature. INCLUSION CRITERIA: in vivo human studies. EXCLUSION CRITERIA: animal trials, in vitro studies and case reports. We also excluded other forms of 'alternative medicine' such as reflexology, acupuncture and other homeopathic remedies. RESULTS: Lack of common outcome measures prevented a formal meta-analysis. Three studies on the effects of spirulina in allergy, rhinitis and immunomodulation were found. One was a double-blind, placebo, randomised, controlled trial (RCT) of patients with allergic rhinitis, demonstrating positive effects in patients fed spirulina for 12 weeks. The other two studies, although non-randomised, also reported a positive role for spirulina in mucosal immunity. Regarding the use of Ginkgo biloba in tinnitus, a Cochrane review published in 2004 showed no evidence for this. The one double-blind, placebo-controlled trial that followed confirmed this finding. Regarding the use of Vertigoheel in vertigo, two double-blind RCTs and a meta-analysis were identified. The first RCT suggested that Vertigoheel was equally effective in reducing the severity, duration and frequency of vertigo compared with betahistine. The second RCT suggested that Vertigoheel was a suitable alternative to G. biloba in the treatment of atherosclerosis-related vertigo. A meta-analysis of only four clinical trials confirms that Vertigoheel was equally effective compared with betahistine, G. biloba and dimenhydrinate. Regarding multivitamins and sinusitis, two small paediatric pilot studies reported a positive response for chronic sinusitis and otitis media following a course of multivitamins and cod liver oil. Regarding bromelain (pineapple enzyme) and sinusitis, one randomised, multicentre trial including 116 children compared bromelain monotherapy to bromelain with standard therapy and standard therapy alone, for the treatment of acute sinusitis. The bromelain monotherapy group showed a faster recovery compared with the other groups. CONCLUSION: The positive effects of spirulina in allergic rhinitis and of Vertigoheel in vertigo are based on good levels of evidence, but larger trials are required. There is overwhelming evidence that G. biloba may play no role in tinnitus. There is limited evidence for the use of multivitamins in sinus symptoms, and larger randomised trials are required.

Bromelains↗
PubMed1997

A postmarketing study of flunarizine in migraine and vertigo.

This prospective, open multi-centre study on flunarizine focused on the risk/benefit ratio of the use of flunarizine in the prophylaxis of migraine and in the treatment of vertigo, due to disorder of the vestibular system. The assessment of risks focused on the incidence of new events of depression and/or extrapyramidal syndrome during flunarizine treatment. For migraine, flunarizine was compared to propranolol in 686 patients; for vertigo, flunarizine was compared to betahistine in 198 patients. The incidence of depression during follow-up in this study was significantly higher in the flunarizine group than in the propranolol group in the condition of migraine. There were no observations of an extrapyramidal syndrome. There was a suggestion that flunarizine has more benefits than propranolol in the condition of migraine, and that betahistine has more benefit than flunarizine in the condition of vertigo. Differences in dosages could possible explain these differences.

Adult↗
PubMed1976

[Medical treatment in Menière's disease (author's transl)].

They are different methods of medical treatment in Menière's disease. 1. The dehydration of the hydrops by diet, diuretics, hypertonic solutions and glycerol. 2. Improvement of the blood supply by carbon dioxide, by myotropic and neurotropic vasodilators or by decreasing the blood viscosity and by medical or surgical paralysis of the sympathetic nerve. The optimistic results seen by acupuncture or neural therapy are not confirmed. - Experimental and double blind studies with betahistin (vasomotal) showed a significant effect in improving the blood circulation of the inner ear and the symptoms of Menière's disease. 3. Sedatives especially neuroleptics and tranquilizers were successful only by suppressing the symptoms, but are not a causal treatment. The same mechanism is supposed for procain and lidocain. 4. Partial destruction of the inner ear has been produced by local application of anesthetics or ototoxic antibiotics. These methods succeed in relieving vertigo and save the hearing in most cases.

Anesthetics, Local↗
PubMed1982

Synergy among agents inhibiting granulocyte aggregation.

Recent evidence suggests complement (C) -stimulated granulocytes (PMNs) are important in a variety of diseases, including shock and myocardial infarction (MI). Corticosteroids inhibit PMN response to C and show promise in some studies of shock and MI, but their use has not become routine for several reasons. Synergy was sought among agents inhibiting PMN aggregation in vitro in response to activated C: methylprednisolone (MP), with a 50% inhibitory dose (AD50) of 0.6 mg/ml; ibuprofen (IBU), with AD50 of 1.0 mg/ml, and betahistine (BH), with AD50 of 1.6 mg/ml. Simultaneous use of all three agents produced 3.4-fold synergy; 3-fold synergy obtained between IBU + MP and IBU + BH, while 1.5-fold synergy was noted between MP + BH. Further, MP and IBU were at least additive in inhibiting .O2- generation by FMLP-stimulated PMNs and in blocking directed migration. In a preliminary in vivo test of this finding, cats were given MP and IBU--in known individually ineffective doses--immediately prior to coronary artery ligation. Neither MP nor the low dose of IBU chosen limited the size of the resultant MI, while both agents together reduced MI size by 42%. Synergy among these agents suggests that they inhibit PMN function of distinct cellular mechanisms (as yet not elucidated). Further, early in vivo results encourage speculation that such synergy might ultimately be exploited clinically, although such speculation must presently be regarded as preliminary.

Betahistine↗
PubMed1996

Phase transitions of rat stratum corneum lipids by an electron paramagnetic resonance study and relationship of phase states to drug penetration.

In order to relate barrier function to stratum corneum structure and the thermal transitions of corneum lipids, samples from hairless rat skin were investigated by using ESR and drug penetration techniques. The phase transition of stratum corneum lipids was estimated using a deeper probe (16-doxyl-stearic acid) inserted in the lipid bilayers and measuring the rotational correlation time, tau(c). Results of ESR study showed that stratum corneum lipids underwent thermal transitions at 39.3 +/- 1.6 degrees C and 63.6 +/- 2.6 degrees C roughly similar to the data obtained by differential scanning calorimetry measurements. Cholesterol oxidase treatment decreased the fluidity of the lipids at lower temperatures. The treatment of stratum corneum with laurocapram (1%) and isopropyl myristate (IPM, 2%) little changed both phase transition temperatures, although the treatment highly increased the molecular motion of the lipids. The flux (J(s)) of lipophilic drugs (beta-estradiol, indomethacin and betahistine) through the skin was enhanced with increasing temperatures, with an increase in the diffusion constant within skin and a decrease in the lag time. There was a good relationship between log J(s) or log permeability coefficient (K(p)) and 1/tau(c) in the temperature range of 45 to 64 degrees C. The calculated activation energy (delta E) for diffusion of these drugs across skin was 17-40 kcal/mol. Judging from our data, stratum corneum lipids of rat probably exist as the gel, crystalline state below 39 degrees C, the mesomorphic state between 39 and 64 degrees C and the fluid, liquid-crystalline state at temperatures of 64 degrees C or above. These results are in line with the permeability of these lipophilic drugs through the intercellular lipids disordered is highly increased.

Animals↗
PubMed1991

Do H3-receptors participate in the effects of histamine on electrically-evoked contractions of rat vas deferens?

1. The specific effects of histamine were studied on rat vas deferens contractions induced by electrical field stimulation (0.1 Hz, 1 pulse, 1 msec duration, supramaximal voltage). 2. Histamine (5 x 10(-7)-10(-4) M) inhibited the electrically-evoked contractions (EEC). This effect was unchanged after the H1-receptor antagonist diphenhydramine (5 x 10(-6) M) and was decreased after the H2-receptor antagonist cimetidine (10(-5) M). 3. Betahistine, described as H1-agonist (in guinea pig ileum) and H3-autoreceptor antagonist (in rat cerebral cortex) slightly decreased the EEC, but competitively inhibited the histamine effect. 4. The results obtained suggest the existence of a specific third type presynaptic H-receptors in rat vas deferens, which are pharmacologically similar to the presynaptic H3-autoreceptors in rat cerebral cortex.

Animals↗
PubMed2005

Histamine (H3) receptors modulate the excitatory amino acid receptor response of the vestibular afferents.

Although the effectiveness of histamine-related drugs in the treatment of peripheral and central vestibular disorders may be explained by their action on the vestibular nuclei, it has also been shown that antivertigo effects can take place at the peripheral level. In this work, we examined the actions of H3 histaminergic agonists and antagonists on the afferent neuron electrical discharge in the isolated inner ear of the axolotl. Our results indicate that H3 antagonists such as thioperamide, clobenpropit, and betahistine (BH) decreased the electrical discharge of afferent neurons by interfering with the postsynaptic response to excitatory amino acid agonists. These results lend further support to the idea that the antivertigo action of histamine-related drugs may be caused, at least in part, by a decrease in the sensory input from the vestibular endorgans. The present data show that the inhibitory action of the afferent neurons discharge previously described for BH is not restricted to this molecule but is also shared by other H3 antagonists.

Afferent Pathways↗