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At least 73 records · Page 4Linked to original sources
PubMed2003

Comparative single- and multiple-dose pharmacokinetics of levodopa and 3-O-methyldopa following a new dual-release and a conventional slow-release formulation of levodopa and benserazide in healthy volunteers.

The objective was to assess the single- and multiple-dose pharmacokinetics of levodopa and 3-O-methyldopa following administration of a new dual-release and conventional slow-release formulation of levodopa/benserazide in the dose ratio of 4:1. In an open-label, two-way cross-over study, 20 healthy volunteers were randomized to receive first either Madopar DR or Madopar HBS for 8 days. Then they crossed over to the other formulation. A first dose of 200 mg levodopa and 50 mg benserazide ('250' mg) was given on day 1, '125' mg t.i.d. on the subsequent 6 days (days 2-7), followed by '250' mg on day 8. The two treatment periods of 8 days were separated by a wash-out period of at least 7 days. Blood samples were taken at specific times over a 12-hour period (day 1) or a 36-hour period (day 8). Plasma concentrations of levodopa and 3-O-methyldopa were measured by high-performance liquid chromatography for pharmacokinetic evaluation. The pharmacokinetics of levodopa after a single-dose administration (day 1) of Madopar DR and Madopar HBS were significantly different as reflected by the respective mean values of maximum plasma concentration (C(max) 1.99 vs. 0.82 mg x l-1), time to reach maximum concentration (t(max) 0.7 vs. 2.6 h) and area under the plasma concentration-time curve (AUC(0- infinity ) 4.52 vs. 3.18 mg x h x l-1). The respective values after multiple doses (day 8) were: C(max) 1.98 vs. 0.93 mg x l-1, t(max) 0.7 vs. 2.3 h and AUC(0-infinity ) 4.84 vs. 3.96 mg x h x l-1. The relative bioavailability (Madopar DR vs. Madopar HBS) was 1.73 on day 1 and 1.32 on day 8. Bioequivalence could not be demonstrated for log-transformed data of AUC and C(max) within a predefined range of 80-125 and 70-143%, respectively. In conclusion, the observed differences in C(max), t(max) and AUC are consistent with a faster rate and higher extent of levodopa absorption after administration of Madopar DR. Statistical evaluation of these kinetic data showed that Madopar DR is not bioequivalent to Madopar HBS.

Adult↗
PubMed2006

Effect of L-dopa decarboxylase inhibitor benserazide on renal function in streptozotocin-diabetic rats.

BACKGROUND/AIMS: Benserazide (BZD), an inhibitor of the dopamine synthesis, abolished the increase in glomerular filtration rate (GFR) following the infusion of a mixed amino acid solution. These results reveal endogenous dopamine as a mediator in the renal response to amino acids. The aim of the present study was to evaluate whether dopamine is also involved in the regulation of glomerular hyperfiltration during the early state of diabetes mellitus (DM). METHODS: Male Sprague-Dawley rats were injected with a single dose of streptozotocin (60 mg/kg i.p.) for induction of experimental DM (n = 7-8/group). Age-matched non-diabetic animals, injected with citrate buffer, served as controls (CON, n = 8/group). Clearance experiments were performed 2 weeks after induction of DM in thiopental-anesthetized rats (80 mg/kg i.p.), which were continuously infused either with BZD (30 microg/min/kg) or vehicle (VHC). RESULTS: Mean arterial blood pressure was around 110 mm Hg and did not significantly differ among the groups. GFR was 0.95 +/- 0.02 ml/min/100 g b.w. in VHC-treated CON. BZD treatment did not significantly change GFR in the CON group (0.92 +/- 0.06 ml/min/100 g b.w.). As expected, glomerular hyperfiltration was observed in diabetic rats infused with VHC (1.24 +/- 0.08 ml/min/100 g b.w.). Treatment with BZD significantly reduced the diabetes-induced increase in GFR to control levels (0.95 +/- 0.05 ml/min/100 g b.w.). CONCLUSION: Our results show that the inhibition of dopamine synthesis prevented the increase in GFR due to diabetic conditions, indicating that endogenous dopamine is involved in the regulation of DM-induced changes in renal hemodynamics.

Animals↗
PubMed1987

Single-dose studies of a slow-release preparation of levodopa and benserazide (Madopar HBS) in Parkinson's disease.

The clinical effects and pharmacokinetic profiles of single doses of Madopar HBS were compared with those of standard Madopar in two studies in patients with Parkinson's disease and 'on-off' fluctuations. In the first study, 10 fasting patients received equivalent doses (200 mg levodopa plus 50 mg benserazide) of each preparation. The clinical response to Madopar HBS was delayed and brief; the relative bioavailability was only 50%. In the second study in 7 non-fasted patients, the effects of 3 capsules of Madopar HBS 125 were compared with those of 2 capsules of standard Madopar 125. Delay to turn on was longer with HBS, but duration of time on, and delay to turn off, were longer with this preparation. The area under the concentration-time curve for plasma levodopa was greater with HBS, and the maximum levodopa concentration was similar to, but achieved later than standard Madopar.

Administration, Oral↗
PubMed1987

[Controlled release levodopa-benserazide and changes in efficacy during treatment of Parkinson's disease].

Twenty-five patients, 12 men and 13 women, 42 to 79 years (mean 62) were studied to determine possible interest of a controlled release preparation of L. dopa combined with benserazide. All patients were experiencing fluctuations in efficacy over the last 8 +/- 4 years. Their Parkinson disease was of long duration, (16 +/- 5 years), severe (Hoehn and Yahr's stages III to V) and treated with L. dopa for 12 +/- 4 years. Results were evaluated in the short, medium and long term. During the initial period the new treatment was substituted for previous therapy on a dose for dose basis. Long term (300 days) results showed that "end of dose" fluctuations had been improved in 40 p. 100 of cases without concomitant reduction in therapeutic effects, duration of "ON" periods progressing by 60%. The frequency of drug intake was unaltered but daily dosage could be increased by 30% without increasing severity of abnormal movements to a similar degree. The administration of this new presentation can be recommended, especially when frequent fluctuations compromise long term therapeutic effects.

Adult↗
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↗
PubMed1979

Dose and sex related effects of benserazide on prolactin secretion.

Benserazide, given orally at various doses ranging from 10 to 125 mg. to healthy women aged 21 to 33 years induces a dose related increase of prolactin titres in serum. When 125 mg are administered the percent increase of the hormone is larger in women than in men.

Adult↗
PubMed1982

[Regression of the cerebellar syndrome under long-term administration of 5-HTP or the combination of 5-HTP and benserazide. 26 cases quantified and treated using computer methods].

A quantitative evaluation of cerebellar ataxia, with an ataxia score (total, static, kinetic) and the measurement of objective values related to the major symptoms, is proposed. 21 patients with heredo-ataxias were treated for 12 months with high doses (16 mg/kg/day) of D-L-5-HTP, L-5-HTP or the association D-L-5-HTP (16 mg/kg/day)-Benserazide(6 mg/kg/day). A computerized processing of the data obtained by regular examination was performed. The ataxia showed a significant regression at the 12th month, mainly in the static performances and in the speed of speech. L-5-HTP appeared to be more active than D-L-5-HTP. The regression of the cerebellar ataxia was also observed in non degenerative conditions such as multiple sclerosis and surgical injury of the anterior lobe vermis, showing that 5-HTP was active on the cerebellar syndrome in general. The regression of the cerebellar ataxia was very slow in inherited diseases and continued for 2 or 4 months after the treatment stopped. A serotoninergic cerebellar control of motricity is discussed.

5-Hydroxytryptophan↗
PubMed1982

The effect of carbidopa and benserazide on human plasma 5-hydroxytryptophan levels.

Peripheral aromatic amino acid decarboxylase inhibitors increase human plasma 5-hydroxytryptophan (5-HTP) levels. However the 5-HTP, which is synthesized in the intestine, is not present in a sufficient quantity to influence brain 5-HT to any significant degree. Thus, peripheral decarboxylase inhibitors are unlikely to affect brain 5-HT function via 5-HTP which is synthesized peripherally.

5-Hydroxytryptophan↗