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Biomedical subjects

C Harvengt

Publications and source records attributed to C Harvengt.

At least 109 records · Page 6Linked to original sources
PubMed1984

Ritodrine serum levels: influence of dose and route of administration.

Serum levels of ritodrine were measured by radio-immunoassay both after single and during chronic administration. In 50 non-pregnant women, the maximum ritodrine levels found after a single dose of 10 mg p.o. were 7.4 +/- 4.7 (ng/ml, +/- SD, n = 10); after 20 mg p.o.: 23.8 +/- 5; after 10 mg i.m.: 30.7 +/- 8.2; after 9.3 mg i.v.: 34.7 +/- 5.5; and after 18 mg i.v.: 75.1 +/- 20.7. Ritodrine determinations during chronic intravenous infusion in 116 pregnant women, at one of the seven infusion rates, showed that the serum steady-state ritodrine levels were proportional to the infusion rates below 400 micrograms/min; above that rate the ritodrine levels flattened out. In 91 pregnant women the ritodrine serum levels were measured at one of a number of different time intervals during chronic oral administration of 5 mg (n = 52) or 10 mg (n = 39) every 4 h. During the chronic oral administration of 10 mg every 4 h, the mean ritodrine levels ranged between 14.3 ng/ml at the peak and 4.6 ng/ml just prior to the subsequent dose. For rapid and controlled tocolysis, intravenous infusion is the most appropriate method; intramuscular administration has no obvious advantage. In this respect, a daily dose of 60 mg, 6 X 10 mg, administered by oral route is probably too low; moreover, the bioavailability of the drug by this route was quite different in two volunteers. Although the absolute bioavailability of the drug was estimated in only a small group of volunteers, consistent results (around 40%) were obtained with the 20-mg oral formulation.

Administration, Oral↗
PubMed1983

Effects of clofibrate, bezafibrate, fenofibrate and probucol on plasma lipolytic enzymes in normolipaemic subjects.

Ten male, normolipaemic, non-obese subjects were given clofibrate 2 g daily, fenofibrate 300 mg daily, bezafibrate 600 mg daily and probucol 1 g daily for eight days, in a crossover study with a wash-out period of 4-8 weeks between each drug regimen. Clofibrate, fenofibrate and bezafibrate caused a significant decrease in serum triglycerides, total cholesterol and LDL-cholesterol concentrations. Probucol caused a significant increase in serum LDL-cholesterol concentration. Serum HDL-cholesterol concentration was significantly increased by bezafibrate and significantly decreased by probucol. All drugs but probucol led to a significant rise in the activity of the plasma lipoprotein lipase; there was not a significant increase in the activity of plasma hepatic lipase after any drug. The activity of plasma lecithin: cholesterol acyltransferase was significantly increased by fenofibrate and probucol. Analysis of the correlations between serum lipids and plasma lipolytic enzymes suggests that the mechanism of the hypolipidaemic action of clofibrate and bezafibrate might be related to increased catabolism of triglyceride-rich particles; that of fenofibrate and probucol was less clear and might be multifactorial in origin.

Adult↗
PubMed1983

Acute cardiovascular and renal changes induced by mitoxantrone in rabbits. A pharmacokinetic approach.

The acute effects of a single i.v. bolus injection of mitoxantrone (MX), a cytostatic drug, on mean arterial pressure (MAP), left ventricular pressure (LVP), dp/dtmax and ECG, were investigated at different doses (1,2,3,5 and 10 mg/kg) in conscious rabbits. Low values of MAP, LVP and dp/dtmax and increased heart rate were observed at 2 h after injection at all dose levels exceeding 1 mg/kg. Plasma kinetics and urinary elimination of MX were determined by high-pressure liquid chromatography (HPLC) and appraised at two dose levels (1.5 mg/kg and 3 mg/kg). MX plasma decay curve at both doses could be fitted to a curve with three exponential components, with an average elimination (3rd component) half-life of about 3.5 h (1.5 mg/kg) and about 5 h (3 mg/kg), respectively. Renal failure was observed in 3 mg/kg-dosed rabbits (elevation of BUN and plasma creatinine, anuria), and resulted in a considerable delay in the MX plasma decay and in a depressed urinary elimination of MX. All but one rabbit died within 24 h. The 1.5 mg/kg-dosed rabbits survived till 24 h, without signs of renal failure, with a 24 h urinary MX recovery of 20%.

Animals↗
PubMed1983

Relative acute cardiovascular toxicity induced by maprotiline, mianserin and nomifensine in conscious rabbits.

The relative acute cardiovascular toxicity among three novel antidepressants: maprotiline, mianserin and nomifensine, has been assessed in conscious rabbits ip injected at 50 mg/kg, throughout a 150 min observation period. No death was observed in mianserin rabbits (n = 6), but 3 in the maprotiline rabbits (n = 8) and 1 death in the nomifensine group (n = 8), within the 2 hours. Cardiac output and renal blood flow were determined by the radioactive Sephadex microspheres method. Cardiac output values were significantly lowered (-29%) at 120 min only in mianserin rabbits, whereas renal blood flow values were reduced by 46.8% (mianserin, 35.8% (maprotiline) and 28% (nomifensine) at 120 min. In mianserin and maprotiline rabbits left ventricular pressure and mean arterial pressure fell significantly, but remained unchanged in nomifensine group. ECG disturbances consisting of ventricular and supraventricular extrasystoles were seen in all the injected rabbits, but QRS widening and right bundle branch block were solely observed after maprotiline and mianserin. Nomifensine rabbits experienced severe seizures with hypocapnia and metabolic acidosis. The drug myocardial/plasma ratio ranged between 59.3 (maprotiline) 13.25 (mianserin) and 0.92 (nomifensine). A rise in plasma catecholamines (epinephrine) was documented after mianserin but not after nomifensin and maprotiline. Nomifensine exhibited much lesser cardiotoxicity than mianserin and maprotiline at this dose (50 mg/kg), but induced more convulsions.

Animals↗
PubMed1983

HDL-cholesterol increase in normolipaemic subjects on khellin: a pilot study.

An evaluation has been made of the action of khellin, a furochromone derivative from Ammi visnaga, at the dose of 50 mg q.i.d. during four weeks, on the plasma lipids of 20 non-obese normolipaemic male subjects after a placebo period of two weeks. The plasma lipids were measured each week and one week after discontinuation of treatment; 14 subjects were evaluable. Plasma total cholesterol and triglycerides concentrations remained unchanged throughout the study, whereas HDL-cholesterol levels were significantly increased from the first week until one week post-medication. A lowering of the LDL-C/HDL-C ratio was shown during the same period. No specific effect on plasma LCAT activity was obtained. Compliance, checked by the plasma khellin determination, was good. Some untoward effects were observed. Nausea and vomiting were responsible for the withdrawal of four volunteers, and elevation of SGOT and SGPT for that of two others. It can be concluded that khellin at this dosage induces an important shift of cholesterol to the HDL fraction which is maintained until one week post-medication.

Adult↗