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At least 19 recordsLinked to original sources
PubMed1978

The effects of a decarboxylase inhibitor, benserazide, on both thermoregulation and chlorpromazine-induced hypothermia in rats.

Intraperitoneal administration of a peripheral decarboxylase inhibitor benserazide (Ro4-4602) to unanesthetized rats produced alterations in body temperature which depended on ambient temperature. In the cold, hypothermia was brought about by a decrease in metabolic heat production. At room temperature, a dose-dependent hypothermia was preceded by a slight hyperthermia. The hypothermia was due to an increase in skin temperature (tail) and a decrease in metabolic heat production, while the hyperthermia was due to a decrease in skin temperatures (both tail and footsole) and an increase in metabolic heat production. In the heat, hyperthermia responses to benserazide were associated with decrease in skin temperature (both tail and footsole). Benserazide treatment produced no significant change in brain 5-HT content. Chlorpromazine-induced hypothermia was greatly enhanced after pretreatment of the animals with benserazide at room temperature (22 degrees).

Animals↗
PubMed1977

A controlled study of a dopa decarboxylase inhibitor (benserazide) in the treatment of schizophrenic patients.

In a double-blind controlled study lasting 6 weeks, 32 schizophrenic patients were randomly assigned to one of two treatments: chlorpromazine or benserazide, a dopa decarboxylase inhibitor. Results on each measure were subject to multifactorial analysis of covariance. Benserazide did not appear to be as effective an antipsychotic medicaiton as chlorpromazine. In fact, chlorpromazine was significantly better on measures of tension, excitement, hallucinatory behavior, thinking disturbance, social interest, and drop-out rate. At the relatively low dosages used in this study, it would seem that benserazide had little effect on the cerebral dopa decarboxylase, and it would be worthwhile trying higher dosages.

Adult↗
PubMed1979

Levodopa with benserazide or carbidopa in Parkinson disease.

Plasma levodopa and therapeutic responses to treatment with levodopa in combination with benserazide or carbidopa were studied in 49 patients with Parkinson disease not previously treated with levodopa in a blind randomized crossover trial. The treatment periods were 12 weeks; similar dosage schedules were used, with doses that induced equal levels of plasma levodopa in both combinations. In pretrial studies of plasma levodopa responses, 200 mg of levodopa and 50 mg of benserazide was equal to 250 mg of levodopa combined with 25 mg of carbidopa. Equal plasma levodopa responses to both combinations were also found during the trial. There was no significant difference between the treatment groups in beneficial effects on parkinsonian disability and individual symptoms or in the frequency of involuntary movements. However, nausea and vomiting occurred significantly more often during treatment with levodopa and carbidopa than during treatment with levodopa and benserazide. This difference was probably due to inadequate inhibition of peripheral decarboxylase inhibitor by the 1:10 ratio of carbidopa to levodopa.

Benserazide↗
PubMed1979

Study on the reproducibility of human prolactin response to sulpiride, benserazide, insulin hypoglycaemia and arginine infusion.

In order to evaluate the spontaneous variability of prolactin (PRL) release in response to various stimuli applied repeatedly on different occasions, groups of 5 to 12 subjects each underwent consecutive identical tests with one of the following stimuli applied at 3-6 days' intervals: sulpiride (100 mg im), benserazide (50 mg po), insulin hypoglycaemia (0.1 U/kg b. w. iv) and arginine infusion (25 g iv in 30 min). When repeated in the same subjects, arginine and benserazide yielded superimposable results. In contrast to this, insulin hypoglycaemia yielded significantly lower PRL release, while the PRL response to the second sulpiride test was significantly higher than to the first one. When an interval of 10 days was left between two consecutive sulpiride tests, an identical PRL release was observed. These results indicate that arginine and benserazide are reproducible tests for PRL secretion and it is possible that the decreasing effect of insulin hypoglycaemia on PRL release is due to the stressful effect of the stimulus. Finally, sulpiride probably enhances both PRL release and synthesis thus making greater amounts of PRL available to a subsequent stimulus. Since some of the above stimuli are usual tools for the study of the neuroendocrine control of PRL secretion, our findings suggest that caution appears necessary in attributing to any (neuroactive) drug an effect which might be merely due to a lack of reproducibility of the stimulus employed.

Adult↗
PubMed1976

[Attempt at potentiation of the action of L-dopa on the secretion of growth hormone by benserazide, disulfiram and propranolol].

Two tests of stimulation of growth hormone secretion were performed in 3 groups of normal children. In the first test L-Dopa was used on its own; in the second, L-Dopa was combined with Benserazide (group A), with Disulfirame (group B), or with Propranolol (group C). In group A the mean peak value after L-Dopa was 9.1 +/- 1.6 ng/ml; with the combination of L-Dopa and Benserazide it was 12.4 +/- 2.4 ng/ml. The difference between the means is not significant. In group B the mean peak value after L-Dopa was 8.9 +/- 3.6 ng/ml; with the combination of L-Dopa and Disulfirame it was 14.5 +/- 4.4 ng/ml. The difference is not significant. In group C the mean peak value after L-Dopa was 9.8 +/- 2.6 ng/ml; with the combination of L-Dopa and Propranolol, it was 10.1 +/- 1.9 ng/ml. Again the difference is not significant. These findings do not provide evidence in favour of the effect of L-Dopa on the secretion of growth hormone being facilitated by an inhibitor of L-Dopa decarboxylase (Benserazide) or of Dopamine beta hydroxylase (Disulfirame), or by a beta blocking agent (Propranolol). The mechanisms of action of L-Dopa and of the various combinations studied are discussed.

Adolescent↗
PubMed1975

Levodopa alone and in combination with a peripheral decarboxylase inhibitor benserazide (Madopar) in the treatment of Parkinson's disease: A controlled clinical trial.

A combination of levodopa and the extracerebrally acting decarboxylase inhibitor benserazide (ratio 4:1) (Madopar), was compared with levodopa alone in a controlled double-blind clinical multicenter trial on 94 patients with Parkinson's disease. During 4 months of therapy levodopa + benserazide proved superior to levodopa on several accounts. Nausea and vomiting occurred with statistically significant less severity and frequency. Clinical improvement expressed through improvement in Webster rating occurred sooner and was all together greater. The treatment schedules did not differ with regard to other side effects, in particular involuntary movements and reduction in supine blood pressure. Neither treatment seemed to influence liver function, renal function and hematological parameters.

Adult↗
PubMed1976

Comparison of levodopa with carbidopa or benserazide in parkinsonism.

The therapeutic efficacy and side-effects of two preparations of levodopa with extracerebral decarboxylase inhibitors have been compared in 19 patients with idiopathic parkinsonism in a blind randomised crossover trial. The mean daily dose of levodopa was 658 +/- 64 mg/day (mean +/- S.E.M.) when given together with carbidopa 66 mg/day and 605 +/- 59 mg/day when levodopa was combined with benserazide 151 mg/day. There was no significant difference between the treatment regimens either in beneficial effects on parkinsonian symptoms and signs or in the adverse effects of levodopa assessed by a clinical observer unaware of the treatment given. Of the 19 patients studied, 9 preferred the carbidopa preparation, 8 preferred the benserazide preparation, and 2 had no preference. It is concluded that there is no significant difference in therapeutic effects or adverse reactions between the two commercially available decarboxylase inhibitor-containing preparations. Central-nervous-system actions and side-effects depend on the daily dose of levodopa, regardless of the different ratios of decarboxylase inhibitors to levodopa.

Aged↗
PubMed1979

Lack of counteracting effect of liposomes on benserazide-induced hyperprolactinemia.

Benserazide induces an increase of serum prolactin in man, possibly as the result of an impairment of the dopamine effect on the pituitary and/or on the outer median eminence caused by the inhibition on L-dopa decarboxylase. On the other hand, liposomes obtained from bovine brain cortex phospholipids reduced serum prolactin possibly through an effect of phosphatidylserine on dopamine biosynthesis at the level of tyrosine hydroxylase. Benserazide, given orally (125 mg) to 5 normal subjects, induced an increase of serum prolactin that did not change when 300 mg of phospholipid liposomes were given intravenously 60 min later. An increase of L-dopa synthesis does not seen to be capable to overcome the effects of the decarboxylase inhibition.

Adult↗
PubMedDate not supplied

Levodopa pharmacokinetics. Alterations after benserazide, a decarboxylase inhibitor.

Plasma levodopa decay curves appeared to be triexponential up to 6 hr after single intravenous injections of levodopa in rats, rabbits, and dogs. After pretreatment of each of these three species with benserazide (Ro-4-4602), a decarboxylase inhibitor, plasma levodopa concentrations declined biexponentially. Administration of benserazide decreased both total plasma clearance and apparent volume of distribution of levodopa, but did not change the rate constant of the terminal phase of the plasma levodopa decay curve. Thus, decarboxylase inhibition failed to alter the plasma half-life of levodopa.

Animals↗
PubMed1979

Benserazide induces migraine attacks. Irrelevance of concomitant hyperprolactinemia.

Migrainous women underwent acute administration of sulpiride (25 mg i.v.) and benserazide (125 mg per os), both drugs increasing prolactin secretion. A similar increase in prolactin levels was found following the administration of the two drugs. A typical migraine attack was observed only in the 4 women given benserazide. These data, though being preliminary, stress the scarce or irrelevant role of prolactin in the pathogenesis of the migraine attack.

Adult↗
PubMed1976

Cardiovascular responses to acute hypoxia in dogs pretreated with benserazide and L-DOPA.

In the control dogs, hypoxia induced different hemodynamic modifications (i.e. an increase of arterial blood pressure, heart rate, cardiac output, regional blood flow) which seem to be related to a release of epinephrine. Pretreatment with benserazide (20 mg/kg i.v.) and L-Dopa (50 mg/kg i.p.) either lessened or completely suppressed any sign of sympathetic stimulation. These results suggest that chemoreceptors are centrally inhibited as had been previously proved for baroreceptors.

Animals↗
PubMed1979

Niacin depletion in Parkinsonian patients treated with L-dopa, benserazide and carbidopa.

1. Benserazide and carbidopa, decarboxylase inhibitors used in the treatment of Parkinson's disease, have been shown to inhibit the enzyme kynurenine hydrolase in rat and mouse liver. This results in reduced synthesis of nicotinamide coenzymes from tryptophan, and hence an increased reliance on dietary niacin. 2. Pellagra might be expected as a result of this inhibition of endogenous synthesis of nicotinamide nucleotides, but has not been reported in patients treated with either drug. 3. The urinary excretion of N1-methyl-nicotinamide, a product of nicotinamide nucleotide metabolism, is considerably reduced in patients treated with dopa alone or in combination with an inhibitor of peripheral dopa decarboxylase, to as low as 40% of the control value. This means that many of these patients could be classified as 'at risk' of niacin deficiency, even if not frankly deficient. 4. Patients treated with dopa plus a decarboxylase inhibitor, but not those treated with dopa alone, also show a reduced excretion of xanthurenic acid, and an increased excretion of kynurenine, as would be expected after inhibition of the kynurenine pathway, and possibly indicative of marginal vitamin B6 deficiency.

Adolescent↗
PubMed1977

Possible mechanism of adverse reaction following levodopa plus benserazide treatment.

1 Rats treated for seven days with seryl-trihydroxybenzylhydrazine (benserazide), and inhibitor of peripheral aromatic L-amino acid decarboxylase (500 mg/kg, daily, i.p.) alone or in combination with L-DOPA methylester (500 mg/kg, daily, i.p.) for seven days showed a moderate but significant decrease of liver aldehyde dehydrogenase (ALDH), without accompanying change in alcohol dehydrogenase (ADH) activity, compared with saline-treated controls. 2 Administration of L-DOPA methylester (500 mg/kg, daily, i.p.) alone for seven days had little effect on liver ADH or ALDH. 3. The combined treatment might be conducive to the in vivo formation of L-DOPA-derived tetrahydroisoquinoline derivatives which might be implicated in L-DOPA produced adverse effects.

Alcohol Oxidoreductases↗
PubMed1977

Bromocriptine alone or associated with L-dopa plus benserazide in Parkinson's disease.

Twenty-six patients affected by Parkinson's disease were treated with a 2-Br-alpha-ergocriptine (CB 154): 14 cases were given CB 154 alone, and 12 were given CB 154 along with L-dopa plus benserazide (Madopar). Both CB 154 and combined therapy (CB 154+Madopar) induced a significant improvement in total disability score, tremor, rigidity, akinesia, self-sufficiency, and some motor performance tests (dynamic tests). No significant difference was found between results obtained with CB 154 therapy and with Madopar treatment, while the improvement induced by combined therapy (CB 154+Madopar) was significantly higher than that obtained by Madopar alone. The averse reactions caused by CB 154 alone or associated with Madopar are similar to those observed during other dopaminergic treatment. CB 154 alone or combined with Madopar appears to be a useful advance in the management of Parkinson's disease.

Aged↗
PubMed1979

[The combined treatment of Parkinson's disease with L-dopa plus decarboxylase inhibitors (carbidopa, benserazide) (author's transl)].

An open cross-over study of 20 patients with Parkinson's disease performed with two drugs containing L-dopa and a peripheral aromatic amino acid decarboxylase inhibitor (benserazide, carbidopa) confirmed the conclusions reached in other clinical trials that this combined treatment of Parkinson's disease is the most effective form of drug therapy available at present. With both drugs, Madopar or Sinemet, an optimum therapeutic result was obtained with relatively small doses of L-dopa (the reduction in L-dopa dosage amounting to about 80%). A loss of efficacy with both drugs, which has observed during long-term treatment of patients with Parkinson's disease, could be avoided by switching the patients from Sinemet to Madopar and vice versa. Determination of L-dopa in the plasma demonstrated that with either drug similar plasma levels of L-dopa were achieved during clinically effective treatment.

Aged↗