Biomedical subjects

M Volz

Publications and source records attributed to M Volz.

29 records · Page 2Linked to original sources

PubMed1988

Pharmacokinetics of amlodipine in renal impairment.

The pharmacokinetics of amlodipine was studied in 27 subjects with renal function ranging from normal to dialysis-dependent. Amlodipine (as a single 5-mg capsule) was administered once daily for 14 days and its plasma concentrations were measured by gas chromatography during and after treatment. Renal impairment had little or no effect on the pharmacokinetics of amlodipine. The elimination half-life was of the order of 50 h, similar to previously observed values, and did not vary with differences in renal function. Steady-state predose concentrations were observed after the ninth dose. Accumulation of amlodipine to steady-state levels was not significantly different from that expected on theoretical grounds and did not significantly change with renal function. These results suggest that once-daily administration of amlodipine is suitable for all degrees of renal function and that dosage adjustment is not necessary in renal impairment.

Adult↗

PubMed1988

[Hemodynamic, anti-ischemic, metabolic and neurohumoral effects of enoximone (MDL 17,043) in patients with coronary disease].

The hemodynamic, anti-ischemic, metabolic, and neurohumoral effects of the phosphodiesterase inhibitor enoximone were investigated in 17 patients (mean age 58 +/- 2 years) with coronary heart disease as established by coronary angiography and positive exercise tests after i.v. application of 0.75 mg/kg body weight. Whereas administration of enoximone resulted in a significant increase in heart rate from 75 +/- 17 to 83 +/- 14 per minute (p less than 0.01), exercise heart rate, blood pressure and myocardial oxygen consumption did not change significantly (p greater than 0.05). At rest, enoximone led to a significant decrease of mean right atrial pressure from 5.7 +/- 2.3 to 3.8 +/- 1.2 mm Hg (p less than 0.01). During exercise there was a significant fall in pulmonary pressure (PAm from 40 +/- 7 to 24 +/- 7 mm Hg, p less than 0.001; PCm from 24 +/- 7 to 14 +/- 6 mm Hg, p less than 0.001) caused by preload reduction and concomitant inotropic increase; there was also a significant rise in cardiac output from 12.7 +/- 5 to 13.8 +/- 5 mm Hg (p less than 0.01) and a decrease of ST-segment depression from 1.97 +/- 0.76 to 0.53 +/- 0.51 mm (p less than 0.001). With improved peripheral and probably coronary blood flow, a concomitant decrease of the metabolic ischemic markers was detected during exercise (potassium 4.44 +/- 0.29 vs. 4.31 +/- 0.30 mval, p less than 0.05; lactate 19 +/- 9 vs. 18 +/- 7 mg/dl; pH 7.28 +/- 0.27 vs. 7.36 +/- 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1985

Rapid and accurate reversed-phase high-performance liquid chromatographic determination of conjugated bile acids in human bile for routine clinical applications. Therapeutic control during gallstone dissolution therapy.

This paper introduces a new method to detect the taurine and glycine conjugates of five different bile acids (cholic acid, deoxycholic acid, chenodeoxycholic acid, ursodeoxycholic acid and lithocholic acid) in human bile. Advantages of this method are sufficient separation of compounds within a short period of time and a high rate of reproducibility. Using a mobile phase gradient of acetonitrile and water, modified with tetrabutylammonium hydrogen sulphate (0.0075 mol/l), we were able to maximize the differentiation between ursodeoxycholic acid and lithocholic acid, which is of primary interest during conservative gallstone dissolution therapy. Use of this gradient reduced analysis time to less than 0.5 h. Recovery rates for this modified method ranged from 94% to 100%, and reproducibility was 98%, sufficient for routine clinical applications.

Bile↗

PubMed1984

Pharmacokinetics and biotransformation of 2-[N-[(S)-1-ethoxycarbonyl-3-phenylpropyl]-L-alanyl]-(1S,3S, 5S)-2-azabicyclo [3.3.0]octane-3-carboxylic acid (Hoe 498) in rat, dog and man.

After oral administration, 2 mg/kg in rat and dog, 10 mg in man, of the carbon-14-labeled angiotensin I converting enzyme inhibitor 2-[N-[(S)-1-ethoxycarbonyl-3-phenylpropyl]-L-alanyl]-(1S,3S, 5S)-2-azabicyclo[3.3.0]octane-3-carboxylic acid (Hoe 498), absorption (rat 56%, dog 43%, man 56%) occurred rapidly and induced maximum blood levels between 0.25 and 1 h. The radioactivity disappeared from the blood in one or two phases with half-lives of 0.6 h in the rat, 1/3.8 h in dog and 0.5/2.9 h in man. Studies in rats have shown that the radioactivity is distributed rapidly to all tissues. Markedly higher concentrations than in the blood were found in the liver, kidneys, and particularly in the lungs. The elimination from the lungs, which showed the highest concentrations until 5 d after administration, occurred with a half-life of 63 h. In rats, 26% of the dose was excreted with the urine and 71% with the feces. About one third of the dose was eliminated with the bile and about 13% was reabsorbed from the bile. The excretion in the breast milk of rats was low. Placental transfer in pregnant rats was low and transient. The radioactivity recovered from the urine of dogs amounted to 15%, that recovered from the feces amounted to 79%. In man, 56% of the radioactivity was excreted with the urine and less than 40% with the feces. Whereas in rat urine one metabolite dominates, the metabolite patterns in urine and serum/plasma of man and dog - which are very much alike - reveal a different biotransformation with three main metabolites. Unchanged Hoe 498, as well as its dicarboxylic acid and other metabolites appear only in low concentrations in this pattern.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1980

Kinetics and metabolism of pyrazolones (propyphenazone, aminopyrine and dipyrone).

1 Propyphenazone 220 mg was administered orally to volunteers. Maximum plasma concentrations between 1.5 microgram/ml and 3.5 micrograms/ml were found 30 min later. After comparable doses plasma concentrations in dog and rabbit were lower. The distribution volumes were 2 l/kg. 2 The major metabolic route of propyphenazone is demethylation. The main urinary metabolite is the enolglucuronide of N-(2)-demethylpropyphenazone. 3 Aminopyrine is rapidly and almost completely absorbed after oral administration. Maximum plasma concentrations of 10 microgram/ml are reached 1.5 h after a 500 mg dose. The biological half-life is 2-3 h, the relative distribution volume 60% on average, and binding to plasma proteins approximately 15%. 4 Unchanged aminopyrine is only excreted in small quantities. The major routes of metabolism are demethylation (4-methylaminoantipyrine and 4-aminoantipyrine) and acylation (4-acetyl and 4-formylaminoantipyrine). There are other biotransformation products. 5 After oral administration of [14C]-dipyrone 480 mg the maximum serum concentration of 13.4 +/- 0.8 microgram/ml occurred at 1-1.5 hours. 6 Dipyrone was not detectable in serum or urine. Four of seven metabolites were identified, and were identical with the main metabolites of aminopyrine.

Administration, Oral↗

PubMed1979