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PubMedDate not supplied

Rheoencephalographic and other studies of betahistine in humans. IV. Prolonged administration with improvement in arteriosclerotic dementia.

The effects of prolonged betahistine administration were studied in institutionalized geriatric patients with particularly severe and long-standing arteriosclerotic dementia. Thirty received betahistine hydrochloride (SERC) or placebo orally in fixed dosage for six months on a double-blind basis and were followed by ward behavioral and psychometric ratings. Six others received active medication and were additionally followed by intracranial rheoencephalography (IREG). Thirty patients successfully completed the two studies. No adverse effects ascribable to the drug were encountered. The results show that betahistine caused definite, strong, and highly significant cerebral and scalp arterial vasodilation and circulatory improvement and that these caused equally definite, strong, and highly significant global improvement in the patients' dementias. Bethahistine, thus, acts in humans as a potent and efficacious cerebral and peripheral microcirculatory and arterial vasodilator which can significantly improve cerebrovascular insufficiency and any associated dementia, no matter how severe either may be and despite the possible presence of large-vessel disease. These improvements sometimes were detected within two weeks or less, developed rapidly to maxima by about 90 days, and were sustained quite well there-after by continued therapy, They may, however, be drug dependent as they regressed in two patients following withdrawal. Various mechanisms whereby a microcirculatory vasodilator can cause arterial vasodilation are considered. The evidence apparently favors that prolonged microcirculatory vasodilatation can cause secondary passive arterial responses. The possibility that the IREG contains external carotid contamination is again examined. Significant discrepancies between the scalp and IREG effects of bethahistine indicate, however, that the response of any such component was negligible within experimental error and that the component, itself, must have comprised but a small percentage of the IREG. Since the circulatory responses detected by the IREG thus arose essentially completely from the effects of betahistine on the cerebral circulation alone, this appears to be the first direct demonstration that cerebral circulatory improvement can cause improvement in mental function in patients with even severe, longstanding, and apparently clinically irreversible arteriosclerotic dementia and that such improvements can be effected pharmacologically.

Aged↗
PubMed1995

Effects of histamine and betahistine on rat medial vestibular nucleus neurones: possible mechanism of action of anti-histaminergic drugs in vertigo and motion sickness.

The tonic discharge of 71 medial vestibular nucleus (MVN) neurones was recorded in slices of the dorsal brainstem of young adult rats. Bath application of histamine caused a dose-related excitation in 59 of the 71 cells (83%), the remaining 12 (17%) being unresponsive. Dimaprit, a selective H2 agonist, also caused excitation in all 20 cells tested. The histamine-induced excitation and the response to dimaprit were antagonised by the selective H2 antagonist ranitidine, confirming that the H2 subtype of histamine receptor is involved in mediating the effects of histamine on these cells. Triprolidine, a selective H1 antagonist, also antagonised the excitation caused by histamine, at a concentration (0.3 microM) which left the H2 receptor-mediated response to dimaprit unchanged. Thus the excitatory effects of histamine on MVN cells in the rat involve two components mediated through H1 and H2 receptor-linked mechanisms, respectively. Betahistine, a weak H1 agonist and H3 antagonist, had little excitatory action when applied on its own, but significantly reduced the excitation caused by histamine when the two drugs were applied together. The effects of betahistine were consistent with a partial-agonist action at H1 receptors on MVN cells, reducing the excitatory responses to histamine presumably by occupying these receptor sites in competition with the exogenously applied neurotransmitter. This partial-agonist action of betahistine may be an important part of its mechanism of action in the symptomatic treatment of vertigo and motion sickness, since it is likely to occur not only in the MVN but also in many brain regions, including the thalamus and cortex, which express H1 receptors and which are innervated by the hypothalamic histaminergic system. Thus the effectiveness of betahistine and other anti-H1 drugs against motion sickness may be explained by their action in reducing the effects of the excess histamine release induced in such conditions in various brain areas, including the MVN.

Animals↗
PubMed1982

Inhibitory effect of betahistine on polysynaptic neurons in the lateral vestibular nucleus.

Effects of betahistine, an antivertigo drug, were examined on the lateral vestibular nucleus (LVN) neurons of cats anesthetized with alpha-chloralose. Spike generation of monosynaptic LVN neurons elicited by vestibular nerve stimulation remained unaffected with intravenous administration of betahistine up to 5 mg/kg and with iontophoretic application of the drug up to 200 nA. In contrast, the spike generation of polysynaptic I neurons in the LVN was dose-dependently inhibited by intravenous as well as iontophoretic application of betahistine. These results suggest that small doses of betahistine more selectively interfere with synaptic transmission in the polysynaptic I neurons than in the monosynaptic neurons.

Animals↗
PubMed1994

[Inner ear blood flow with betahistine--an animal experiment study].

The influence of the drug Betahistin on the cochlear blood flow (CBF) was checked on 15 guinea pigs (6 controls) (Charles River, BFA 350-450 g) by means of the hydrogen clearance method. The hydrogen clearance measurements were carried out under alpha-chloralose-ethylurethane anaesthesia, artificial respiration with simultaneous control of the electrocardiogram, arterial blood pressure and body temperature. The actual arterial pH-value was checked hourly. Indirect measurement of CBF was carried out in the perilymphatic space (basal turn) before and after intravenous application of Betahistin (vena jugularis externa) (dosage: 0.11 mg/kg/min). The mean arterial blood pressure remained within the 10% range during the experiments. Under Betahistin-treatment the CBF showed an significant increase (p = 0.05). Despite this favourable pharmacological efficiency of Betahistin it must be pointed out that the general application of vasoactive drugs, especially of vasodilative drugs, in the treatment of postulated inner ear blood flow disturbances is presently controversial.

Animals↗
PubMed2000

Betahistine effects on cochlear blood flow: from the laboratory to the clinic.

The development of laser Doppler flowmetry techniques has contributed greatly to the study of cochlear blood flow (CBF). In animal models, intravenous betahistine dihydrochloride clearly increased CBF in a dose-dependent manner. This effect was greater in the cochlear vasculature than in the systemic vascular bed. The effects of betahistine were blocked by the alpha 2-antagonist idazoxan, thus suggesting an interaction between histaminergic and presynaptic adrenergic receptors. This was further supported by studies investigating the effects of electrical stimulation on CBF. Local (round window membrane) application of betahistine did not affect CBF, but had a non-specific effect on cochlear electrophysiology. This indicates that the receptors for betahistine vascular effects in the inner ear are most likely located in the modiolar artery. More recently, laser Doppler flowmetry techniques have been applied to human subjects. It has been shown that intratympanic application of adrenaline affects CBF and that this blood flow is under vigorous sympathetic control. Electrical stimulation has also been used to obtain measures of dynamic responsiveness in human subjects. This results in an increase in CBF, which is dependent on the intensity of the stimulation. Preliminary evidence indicates that this procedure can provide a standardized measure of the dynamic properties of CBF and may provide a means to differentially identify patients with compromised vasculature.

Adrenergic Agonists↗
PubMed2000

Betahistine reduces the resting firing rate of vestibular receptors in the frog.

Although betahistine is widely used in the treatment of vertigo, it remains unclear whether it directly affects the vestibular system at the peripheral level. The effects of betahistine were therefore assessed in an isolated preparation of frog semicircular canal. Betahistine was administered either in the endolymphatic or the perilymphatic fluid and the ampullar receptor potential and mass nerve discharge were recorded at rest and during mechanical stimulation. Endolymphatic administration was without effect. In contrast, perilymphatic administration resulted in a marked reduction in ampullar receptor resting discharge, although the mechanically evoked responses were only slightly affected. As vertigo is generally caused by sudden and uncontrolled changes in the resting discharge of vestibular receptors, the ability of betahistine to reduce the resting firing rate of vestibular receptors is thought to contribute to its anti-vertigo actions.

Animals↗
PubMed1982

Long-term evaluation of the treatment of Menière's disease with betahistine HCl.

Long-term evaluation of patients treated continuously for a period of 12-14 years with betahistine HCl shows a success rates of more than 80%. Many of these patients had various other kinds of therapy before betahistine HCl treatment to no avail. It seems to us that betahistine HCl is only a basic long-term treatment which has no habituation and still is active in controlling Menière's disease even after a long-term period. Other drugs such as antihistamine, phenothiazines, vitamins and tranquilizers only produce a symptomatic treatment. Betahistine HCl produces no modification or effect on the evolution of deafness.

Audiometry↗
PubMedDate not supplied

Distribution of cardiac output in dogs during intravenous infusion of betahistine.

Cardiac output (CO), arterial blood pressure (ABP), heart rate (HR), blood gases and blood flow (BF) to the brain, heart, kidney and skeletal muscles and other cephalic tissues in five dogs were studied before and at 30 minutes of betahistine infusion (0.12 to 0.2 mg per minute per kilogram). The particle distribution method using radioactive labeled 141Ce (15 mu) and 85Sr (15 mu) microspheres was utilized to quantitate and assess BF and CO. In the five dogs, the increase in CO averaged 20.8%, ABP remained constant, and HR increased in all but one exception where it decreased slightly concomitant with a decrease in Paco2. Brain BF increased (+ 29.6%) in the dogs whose Paco2 reamined constant. The BF increased to the heart (25.4%) and skeletal muslce (80%), while BF to the kidney and other tissues did not change. The change in HR appears to account for the change in CO. The dilating effect of betahistine on blood vessels, in the skeletal muscle, brain and heart could reduce peripheral resistance and decreace ABP. Thus, the increase in HR may be mediated through baroreceptor mechanisms rather than by a direct effect of betahistine. In addition, a decrease in Paco2, is more effective for decreasing cerebral BF than betahistine is for increasing blood flow.

Animals↗
PubMedDate not supplied

Comparative responses of the carotid and vertebral arterial systems of rhesus monkeys to betahistine.

A newly developed photoelectric method was used in 5 rhesus monkeys to measure the mean transit time of blood through the carotid and vertebral arteries, together with measurement of the blood flow through the tissues of the fronto-parietal area supplied by the carotid artery and of the cerebellar tonsil supplied by the vertebral artery. Following intravenous administration of betahistine mesylate, a histamine analog, the mean transit times of blood through the 2 arteries were equally shortened by 10%, despite a 20% decrease in the mean arterial blood pressure (P less than 0.05). The cerebral tissue and cerebellar tissue blood flow was increased by betahistine, from 70.4 to 81.4 ml/100g/min and from 73.2 to 84.0 ml/100g/min, respectively. Since histamine has been reported to produce a decrease in cardiac output, the increase in cerebral blood flow confirmed that betahistine is a selective cerebral vasodilating agent. However, by comparing the hemodynamic data for the two cerebral arterial systems, it can be concluded that the responses of the carotid and vertebral arterial systems to the vasodilating action of betahistine were essentially the same in extent.

Animals↗
PubMed1986

A double-blind crossover study comparing betahistine and cinnarizine in the treatment of recurrent vertigo in patients in general practice.

A double-blind crossover study was carried out in general practice in 88 patients with peripheral vertigo of unknown origin to compare the efficacy and tolerance of 12 mg betahistine dihydrochloride and 15 mg cinnarizine. Patients were allocated at random to receive 2 tablets 3-times daily of one or other drug for 3 consecutive months before being crossed over to the alternative medication for a further 3 months. Severity of symptoms was assessed at 4-week intervals using the Clinical Global Impression scale and patients kept a record in a daily diary of the frequency and duration of attacks. Details were also recorded of any side-effects reported. The results were analyzed for 46 patients who completed the 6-month study period. Both drugs were shown to be equally effective in reducing the duration and severity of symptoms. Significantly fewer attacks of vertigo, however, occurred during betahistine therapy. Side-effects were the most common reason for dropping out whilst on cinnarizine (9 patients) and were complained of by 38 patients during the study (16 only when on betahistine, 19 only on cinnarizine, 3 whilst on both drugs). The most frequently reported were drowsiness or lethargy affecting 16 patients on cinnarizine and 7 on betahistine.

Aged↗
PubMed2001

Betahistine in the treatment of vertigo. History and clinical implications of recent pharmacological researches.

A short profile of betahistine and its activity in treatment of Menière's disease and other forms of peripheral vertigo is presented. The clinical efficacy of betahistine is documented by a series of more than twenty controlled clinical studies, performed in the years 1966-2000. Basic researches initially proved that bethaistine acts trough a vasodilating action on inner ear and cerebral blood flow (Suga and Snow, 1969; Martinez, 1972). In the following years this activity was confirmed using the modern laser doppler flowmetry technique (Laurikainen et al, 1998). Further recent studies proved that betahistine acts on the central vestibular histaminergic system as a weak H1 agonist and a strong H3 antagonist (Arrang et al., 1985), improving the process of vestibular compensation (Tighilet et al., 1995) as well as on peripheral labyrinthine receptors, reducing the spontaneous firing rate but not the activity induced by thermal or mechanical stimulation (Botta et al., 1998). More than forty years after its discovery, this series of studies carried out in the second half of the 90s leads to the conclusion that betahistine is a drug which maintains its scientific interest and its pharmacological potential in the treatment of vertigo.

Betahistine↗
PubMed1972

The effect of betahistine on gastric acid secretion and mucosal blood flow in conscious dogs.

In 3 conscious dogs, betahistine (2-(2'-methyl aminoethyl pyridine)) (80 or 160mug kg(-1) min(-1)) increased acid secretion from Heidenhain pouches to 8.8% and 17.6% respectively of the maximal response to histamine. Betahistine also increased mucosal blood flow (radioactive aniline clearance). The ratio of mucosal blood flow to secretion was greater for betahistine than for histamine but the difference between betahistine and histamine was significant in only one of the dogs.

Amine Oxidase (Copper-Containing)↗
PubMed1999

Effect of the H1-histamine receptor agonist betahistine on drinking and eating behavior in pygmy goats.

The effect of different doses of the H1-receptor agonist betahistine (0.9 and 2, 4 and 8 mg/kg b.wt.(0.75)) on water and food intake was investigated in 12 pygmy goats. Intraperitoneal (i.p.) injection of betahistine (2, 4, and 8 mg/kg b.wt.(0.75)) stimulated drinking in a dose-dependent manner. Food intake was decreased after the injection of 4 or 8 mg/kg b.wt.(0.75) betahistine, respectively. The increase in water intake was characterized by an increased draft size and decreased latency to drink. The decrease in food intake at the highest dose tested was characterized by an increased latency to eat and by a decreased meal frequency, and food intake associated to drinking was decreased. In line with previous studies, these results support the hypothesis that food-associated drinking is mediated by stimulation of H1-receptors of histamine in pygmy goats.

Animals↗
PubMed2000

Betahistine, vestibular function and compensation: in vitro studies of vestibular function and plasticity.

Histamine has an excitatory action on rat medial vestibular nucleus neurones in vitro, an effect that is mediated by histamine H1 and H2 receptors. Betahistine, which is a weak agonist at the H1 receptor and a moderate antagonist at the presynaptic H3 autoreceptor, weakly excites medial vestibular nucleus cells but antagonizes their responses to histamine. Experiments were carried out on rat medial vestibular nucleus cells in vitro using slices prepared from animals that had undergone unilateral labyrinthectomy (UL). There was a significant increase in the intrinsic excitability of medial vestibular nucleus cells in the rostral region of the ipsi-lesional nucleus within 4 h post-UL, which was sustained for the following week. These changes in intrinsic excitability of the medial vestibular nucleus neurones were abolished in animals that were not exposed to the secretion of stress hormones that normally occurs following UL. Histamine is also released in response to the stress associated with vestibular dysfunction. It is possible that the beneficial effects of betahistine on vestibular compensation are related to an interaction between histaminergic receptors activated by the parallel release of histamine and the activation of glucocorticoid receptors through the activation of the stress axis. Further study of the interactions between histamine receptors and the activation of the stress axis may be useful in understanding the effects of betahistine on vestibular plasticity.

Adaptation, Physiological↗
PubMed2003

LC-MS-MS analysis of 2-pyridylacetic acid, a major metabolite of betahistine: application to a pharmacokinetic study in healthy volunteers.

1. A sensitive liquid chromatographic-tandem mas spectrometric assay was developed and validated to determine the major metabolite of betahistine, 2-pyridylacetic acid, in human plasma. 2. The analyte was extracted from plasma samples by liquid-liquid extraction and analysed using liquid chromatography-tandem mass spectrometry with an electrospray ionization interface. The method has a lower limit of quantitation of 1 ng ml(-1) fir a 0.5-ml plasma aliquot. The intra- and interday precision (relative standard deviation), calculated from quality control (QC) samples, was less than 10%. Accuracy as determined from QC samples was within +/-7%. 3. The validated method was successfully applied to a pharmacokinetic study of betahistine in healthy volunteers. After oral administration of a single dose of 24 mg betahistine mesylate to 20 healthy Chinese male volunteers, Cmax was 339.4 ng ml(-1) (range 77.3-776.4 ng ml(-1)). The t(1/2) was 5.2 h (range 2.0(-1)-11.4h). The AUC(0-t) obtained was 1153.5 ng ml(-1) h (range 278.5-3150.8 ng ml(-1)). The disposition of the metabolite exhibited a marked interindividual variation. 4. The plasma concentrations of the parent drug were less than 0.5 ng ml(-1), suggesting that it undergoes almost complete first-pass metabolism. The reported two active metabolites were not detected in the plasma of any volunteer. Although there is no evidence that the major metabolite has pharmacological activity, the clinical importance of 2-pyridylacetic acid in humans should be reinvestigated.

Acetates↗
PubMed2005

The effect of betahistine, a histamine H1 receptor agonist/H3 antagonist, on olanzapine-induced weight gain in first-episode schizophrenia patients.

Histamine antagonism has been implicated in antipsychotic drug-induced weight gain. Betahistine, a histamine enhancer with H1 agonistic/H3 antagonistic properties (48 mg t.i.d.), was coadministered with olanzapine (10 mg/day) in three first-episode schizophrenia patients for 6 weeks. Body weight was measured at baseline and weekly thereafter. Clinical rating scales were completed at baseline and at week 6. All participants gained weight (mean weight gain 3.1+/-0.9 kg) and a similar pattern of weight gain was observed: an increase during the first 2 weeks and no additional weight gain (two patients) or minor weight loss (one patient) from weeks 3 to 6. None gained 7% of baseline weight, which is the cut-off for clinically significant weight gain. Betahistine was safe and well tolerated and did not interfere with the antipsychotic effect of olanzapine. Our findings justify a placebo-controlled evaluation of the putative weight-attenuating effect of betahistine in olanzapine-induced weight gain.

Adult↗
PubMed1989

Effect of betahistine dihydrochloride compared with cinnarizine on induced vestibular nystagmus.

The effect of betahistine compared with cinnarizine on induced vestibular nystagmus was evaluated using a rotating chair, in 6 healthy volunteers. The subjects underwent a slow acceleration followed by a sudden stop. Electronystagmograph tracings were taken initially as pretreatment control values, and after betahistine 8 mg t.i.d. and cinnarizine 15 mg t.i.d. had been taken. The duration of nystagmus and average eye speed were measured. No difference was recorded in either parameter between the pretreatment rotation and that following betahistine (P greater than 0.05). A significant difference (P less than 0.05) was seen in the duration of nystagmus during initial acceleration, and in average eye speed following the sudden stop after treatment with cinnarizine.

Adult↗
PubMed1996

Betahistine-induced bronchospasm.

Betahistine is a cerebral vasodilator structurally related to histamine, which stimulates H1 bronchial and vascular receptors. We report the case of a 28-year-old female patient who presented bronchospasm during treatment with betahistine hydrochloride. The prick test was negative. The oral challenge test showed bronchospasm and urticarial lesions. To the best of our knowledge, this is the first case of betahistine-induced bronchospasm reported in the literature. The study carried out failed to reveal the mechanism of the reaction.

Adult↗