Disease relevance of Vasomotal

• To test the effectiveness of betahistine HC1 in reducing the frequency of transient ischemic attacks (TIAs) caused by vertebral-basilar artery insufficiency, we randomly assigned 26 patients with a typical history of the condition to a placebo-drug or a drug-placebo sequence, each sequence lasting two months [1].
• In Ménière's disease treatment strategies range from low-salt diet, diuretics, and betahistine, to intratympanic injection of corticosteroids or gentamicin [2].
• Betahistine is a structural analogue of histamine that is prescribed for the treatment of vestibular disorders such as M??ni??re's disease and the symptomatic treatment of vertigo [3].
• A clinical intolerance to betahistine that gave rise to asthma or bronchospasm was only reported in eight ADRs [3].
• In this review we analyse the safety profile of betahistine based on data obtained during >35 years of worldwide postmarketing surveillance.Until 31 December 2005, 554 adverse drug reaction (ADR) reports with 994 individual signs and symptoms were received by the marketing authorisation holder from worldwide sources and were reviewed and evaluated [3].

Psychiatry related information on Vasomotal

• Rheoencephalographic and other studies of betahistine in humans. IV. Prolonged administration with improvement in arteriosclerotic dementia [4].
• 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 [4].
• Effect of the H1-histamine receptor agonist betahistine on drinking and eating behavior in pygmy goats [5].
• Evaluation of betahistine for the prevention of seasickness: effect on vestibular function, psychomotor performance and efficacy at sea [6].

High impact information on Vasomotal

• 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 [7].
• 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) [8].
• The dilating effect of betahistine on blood vessels, in the skeletal muscle, brain and heart could reduce peripheral resistance and decreace ABP [8].
• Thus, the increase in HR may be mediated through baroreceptor mechanisms rather than by a direct effect of betahistine [8].
• Some success with betahistine has been achieved but the mechanism of this drug's action may be other than vasodilatation [9].

Chemical compound and disease context of Vasomotal

• We report the case of a 28-year-old female patient who presented bronchospasm during treatment with betahistine hydrochloride [10].
• There was no clear difference regarding efficacy between flunarizine and betahistine in the vertigo study [11].
• A double-blind crossover study comparing betahistine and cinnarizine in the treatment of recurrent vertigo in patients in general practice [12].
• As the effects of H1- and H2-blockade, and the possible involvement of H3-receptors, have not been elucidated, we have examined the effects of combinations of cetirizine, cimetidine and betahistine on the response of patients with confirmed schistosomiasis [13].
• Comparator drugs were propranolol in migraine and betahistine in vertigo [11].

Biological context of Vasomotal

• Distribution of cardiac output in dogs during intravenous infusion of betahistine [8].
• Inhalation of an H2 agonist (impromidine) but not of an H1 agonist (betahistine) caused a decrease of neutrophil chemotaxis and of T-lymphocyte proliferation [14].
• In slices from mouse cerebral cortex, betahistine induced [3H]glycogen hydrolysis in a concentration-dependent manner with an EC50 value of 9.0 microM with a maximal effect 57% that of histamine [15].
• The percutaneous absorption of betahistine (BH) from a gel formulation containing negatively charged liposomes of BH was much more than that from the formulation with positively charged ones, with 2-fold higher AUC (p<0.05) [16].
• Food intake was decreased after the injection of 4 or 8 mg/kg b.wt.(0.75) betahistine, respectively [5].

Anatomical context of Vasomotal

• 2-Methylhistamine, N alpha,N alpha-dimethylhistamine and betahistine were partial agonists in both cerebellum and cerebral cortex, but all produced a greater percentage of the maximum response to histamine in cerebellar slices [17].
• 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 [18].
• Extracellular single-unit activity was recorded from the caudal, spinal-projecting region of the vestibular nuclei during tilt of the animal, before and after i.p. injection of betahistine [19].
• [3H]Mepyramine binding to H1-receptors in membranes from guinea-pig cerebellum was inhibited by betahistine with a Ki value of 31 microM [15].
• Betahistine-induced vascular effects in the rat cochlea [20].

Associations of Vasomotal with other chemical compounds

• These increases may indicate that betahistine hydrochloride can also act as an arterial vasodilator in sufficiently high dosage, but they equally may indicate that sufficiently profound microcirculatory vasodilatation can elicit secondary arterial circulatory increases [21].
• In this open, cross-over study, volunteers were randomly allocated to five treatment protocols i.e. (a) histamine 1 microgram i.d.; (b) betahistine 57, 114 and 285 micrograms i.d.; (c) i.d. grass pollen antigen; (d) (c) plus oral betahistine; (e) (c) plus oral betahistine, cetirizine, (H1-blocker) and cimetidine (H2-blocker) [22].
• 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 [18].
• 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 [23].
• 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 [24].

Gene context of Vasomotal

• 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 [25].
• The aim of this study was to determine the effect of betahistine (an H3-receptor blocker with partial H1- and H2-agonism) on the dynamics of the cutaneous hypersensitivity reaction [22].
• The effect of betahistine, a histamine H1 receptor agonist/H3 antagonist, on olanzapine-induced weight gain in first-episode schizophrenia patients [26].

Analytical, diagnostic and therapeutic context of Vasomotal

• This review provides new insights into the basic mechanisms by which betahistine improves vestibular compensation in animal models of unilateral vestibular dysfunction, and elucidates particularly the mechanisms of action of this substance at the level of the CNS [27].
• Also, beta-histine was capable of significantly reducing the size of developing infarcts for up to 120 min after ligation [28].
• Each individual received, in a randomized double-blind study, 3 different single oral dosages of betahistine (8, 16 and 32 mg) on 3 different occasions [29].
• The cerebellar region, which is the most important area involved in vertigo patients with vascular pathology, showed almost complete normalisation of perfusion following Betahistine therapy [30].
• Pre and post betahistine therapy 99m Tc - HMPAO brain spect studies in patients with vertigo [30].

References