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Biomedical subjects

F Belpaire

Publications and source records attributed to F Belpaire.

At least 37 records · Page 2Linked to original sources
PubMed1984

Immunonephelometry of apolipoprotein A-II in plasma.

A quantitative assay based on endpoint immunonephelometry was developed for human apolipoprotein A-II (apoA-II) in plasma or serum. Dilution of plasma samples with a 0.1 mol/L solution of sodium cholate enhanced the quantification. We used either purified apoA-II as the primary standard or plasma as a secondary standard. Results correlated well (r = 0.90) with those by a double-antibody radioimmunoassay for 63 serum samples from both normal and hyperlipemic individuals. The interassay coefficient of variation for the immunonephelometric assay was 7% within a working range between 0.05 and 0.7 microgram of apoA-II per sample (corresponding to a 1500-fold final dilution of serum). No extraction of samples with organic solvent is necessary if the triglyceride concentration is less than 4 g/L.

Apolipoprotein A-II↗
PubMed1984

8-Methoxypsoralen plasma levels and phototoxic effect.

In 8 normal volunteers, the minimal phototoxic dose was determined at 15 min intervals up to 60 min and thereafter every 30 min up to 4 h; 8-methoxypsoralen (8-MOP) was administered as a solution and small additional doses were given during the course of the experiment, so that a more or less predictable and stable plasma concentration was obtained and maintained for about 2 h. Three of the subjects absorbed 8-MOP very rapidly, already reaching plasma concentrations above 200 ng/ml after 15 min; in the other 5, absorption was slower and comparable levels were achieved only after 30 to 90 min. In the fastest absorbers, there was a 15 to 30 min lag between reaching a high plasma level and a low MPD. In the other cases, such a delay was not seen. This suggests that the time to reach peak concentration in the skin is not influenced by changes in absorption rate: simulations based on the classical plasma concentration equations for a two-compartmental model also show this. Afterwards, the skin sensitivity decreased in most cases parallel to the plasma concentrations.

Female↗
PubMed1983

Interaction of antacids with antiarrhythmics. V. Effect of aluminium hydroxide and magnesium oxide on the bioavailability of quinidine, procainamide and propranolol in dogs.

The influence of aluminium hydroxide and magnesium oxide on the oral bioavailability of quinidine, procainamide and propranolol in the dog was investigated. The administration of aluminium hydroxide with a quinidine sulfate capsule causes a significant decrease of maximal plasma concentration (Cpmax) and a shift in tmax (time to reach Cpmax). The area under the curve is not significantly decreased. Administration of magnesium oxide together with a quinidine sulfate capsule or a sustained-release preparation of quinidine bisulfate causes a significant decrease of both Cpmax and the area under the curve. A shift of tmax was observed for the conventional preparation only. The administration of aluminium hydroxide with procainamide hydrochloride diminishes only Cpmax in a significant way. Administration of magnesium oxide together with procainamide hydrochloride has no influence on the different parameters. Administration of aluminium hydroxide or magnesium oxide with propranolol hydrochloride has a significant negative influence on both the Cpmax and the area under the curve.

Aluminum Hydroxide↗
PubMed1983

Peritoneal pharmacokinetics of gentamicin in man.

The peritoneal pharmacokinetics of gentamicin were investigated in patients on continuous ambulatory peritoneal dialysis. Gentamicin was added to the dialyzate, and gentamicin concentrations were measured repeatedly in serum and dialyzate. After administration of a single dose of gentamicin, equilibrium between serum and dialyzate levels is achieved within 24 hours; dialyzate levels of gentamicin are lower and mass transfer coefficients higher in patients with peritonitis. With chronic intraperitoneal gentamicin treatment for peritonitis, steady state serum levels around 4 to 5 mg/l are achieved and otovestibular toxicity should be feared.

Ascitic Fluid↗
PubMed1982

A screening procedure for dyslipoproteinemia in the newborn. Apoprotein quantitation on dried blood spots.

A new screening procedure for the detection of dyslipoproteinemia in the newborn is proposed, based on apoprotein quantitation. Blood is collected by heel-prick in infants 5--7 days after birth--when apoprotein and lipids have reached stable values--and adsorbed on filter paper. Blood spots are eluted with a detergent and apoprotein A-I and B are assayed by immunonephelometry. The apo A-I/B ratio is used as a screening parameter, given its high discriminative power between normals and individuals with cardiovascular disease. The quantitation of the apo A-I/B ratio in blood spots is independent of the volume of the blood spot and of the newborn hematocrit. In a follow-up study, plasma lipid and apoprotein concentrations were assayed in the infants with an apo A-I/B ratio lower than 1.0 at 5 days, and a family study was carried out. On screening 1500, 30 infants gave positive results at birth, and were controlled between 2 and 8 months. In eight families studied, six children had abnormally high cholesterol and apo B values and five children had abnormally low HDL cholesterol and apo A-I concentrations. This screening procedure is a new approach to the detection of familial dyslipoproteinemia in the newborn, as it is based on the quantitation of the apo A-I/B protein ratio, instead of cholesterol, LDL cholesterol or beta-lipoprotein quantitation. It enables a differentiation to be made between various forms of dyslipoproteinemia, leads to a better characterization of various diseases, and decreases the percentage of false positive cases.

Adult↗
PubMed1982

Pharmacokinetics of digoxin in C.A.P.D.

The peritoneal elimination of digoxin during C.A.P.D. was studied in five patients. The plasma half life of digoxin varied from 54 hours to 141 hours. Only 7 to 24 micrograms was eliminated via the peritoneal route during 3 to 4 days C.A.P.D. treatment. The total urinary elimination during the same period ranged from 11 to 57 micrograms. It is concluded that adjustment of dose is not necessary when starting C.A.P.D.

Aged↗
PubMed1982

Plasma apoproteins levels in chronic alcohol abuse.

The plasma lipid and apoprotein concentrations were monitored in a group of 12 patients with chronic alcohol abuse entering an abstinence program for 3 weeks. 6 of them had a normal liver function as expressed by the levels of liver enzymes gamma GT, GOT, GPT, while 6 had elevated plasma liver enzyme concentrations. None had evidence of either cirrhosis or alcohol hepatitis. Patients with abnormal liver enzymes had elevated HDL-cholesterol, apo AI and apo AII concentrations in plasma, with normal total cholesterol and apo 8 concentrations. In the group of patients with normal liver enzyme concentrations, the apoproteins and lipids did not significantly differ from the control group. In the course of the abstinence treatment a parallel decrease of apoproteins, HDL-cholesterol and liver enzyme concentrations was observed. The values normalized after 10-15 days. These data indicate that the effect of alcohol on the plasma apoprotein and lipids occurs mostly in the HDL fraction, that it correlates with the state of hepatic function and that it can be reversed by an abstinence treatment.

Adult↗
PubMed1981

Lidocaine plasma concentrations obtained with a standardized infusion in the awake and anaesthetized dog.

Lidocaine was administered intravenously on several occasions to three healthy mongrel dogs. The lidocaine treatment consisted of an infusion of 0.8 mg/kg/min over 10 min, followed by an infusion of 0.085 mg/kg/min over 3 h. This lidocaine treatment was given once in the awake state and on two other occasions the infusion was started before or during the following anaesthetic regimen: atropine-meperidine premedication, thiopental induction and maintenance nitrous oxide-methoxyflurane anaesthesia. In most instances plasma levels were somewhat higher at the end of the loading infusion (greater than 5 micrograms/ml) than subsequently, but steady-state values were obtained soon after starting the 3-h infusion. There were no striking differences between the plasma profiles and half-lives found in the three series of experiments: mean plasma concentrations of lidocaine during steady state were between 3.5 and 5.0 micrograms/ml and the half-life of lidocaine was 1 to 2 h. Signs of intoxication were not seen in any of the dogs at any stage of the procedures. It is concluded that with the loading and maintenance doses used in this study steady-state values, probably within the therapeutic range, are obtained within a few minutes. The plasma concentrations are not influenced by the anaesthetic regimen used.

Anesthesia↗
PubMed1981

Digoxin-quinidine interaction in the dog.

In seven healthy dogs, digoxin was given as an oral loading dose (0.05 mg/kg/day) on the first day, followed by an oral maintenance dose (0.02 mg/kg/day) during the next 14 days. On the sixth day of digoxin treatment, oral quinidine (200 mg b.i.d.) was added until the tenth day. Plasma concentrations of digoxin and quinidine were measured; in three of the seven dogs ECG and physical signs of digitalis toxicity were evaluated. The average steady state plasma concentration of digoxin increased significantly (P less than 0.01) during quinidine administration (from 1.4 to 2.3 ng/ml). On the days that digoxin was administered without quinidine, none of the dogs vomited nor was anorectic; the PQ-interval increased significantly (P less than 0.01) between 0.01 and 0.03 s. When quinidine was added, vomiting and anorexia occurred but no further increases in the PQ-interval were seen.

Animals↗
PubMed1980

Effect of formulation on dissolution and bioavailability of phenytoin tablets.

Bioavailability of different phenytoin tablets was calculated from saliva phenytoin levels in healthy human volunteers in a single dose study. Tablets containing different excipients and either phenytoin free acid or sodium phenytoin were chose on the basis of an in vitro dissolution rate study of different tablets. Tablets containing phenytoin precipitated with polysorbate 80 showed faster in vitro dissolution and also higher bioavailability than tablets prepared with phenytoin free acid with different excipients. In vivo studies showed that proper formulation of a tablet containing the free acid form of phenytoin can give rise to the same bioavailability than that of sodium phenytoin. In vitro dissolution of the formulation reflected in vivo bioavailability.

Adult↗
PubMed1978

Pharmacokinetics of drugs in rabbits with experimental acute renal failure.

Serum protein binding and serum levels of antipyrine, phenytoin and phenylbutazone were measured in rabbits with acute renal failure induced by uranyl nitrate. The kinetics of antipyrine are not altered in the uraemic rabbit. Serum protein binding of phenytoin and phenylbutazone is decreased and the volume of distribution of total drug is increased. The volume of distribution of free phenytoin is unchanged, that of free phenylbutazone is decreased in acute renal failure. The half-lives of phenytoin and phenylbutazone are unchanged, but the serum clearance is increased in experimental acute renal failure. The intrinsic clearance of free drug, i.e. the ability of the liver enzymes to metabolize the drug, is not altered for antipyrine, is increased for phenytoin and is decreased for phenylbutazone. It is difficult to extrapolate these data obtained in rabbits with acute renal failure to humans in chronic renal failure.

Acute Kidney Injury↗
PubMed1977

Serum binding of quinidine in experimental acute renal failure.

Quinidine serum binding is increased in some patients with acute renal failure, but in animals with renal failure conflicting results were published. Therefore, serum binding of quinidine, papaverine and phenylbutazone was studied by equilibrium dialysis in rabbits and rats with acute renal failure induced either by injection of uranyl nitrate or ligation of the ureters. From the results it appears that, in animals, quinidine binding changes are different according to the model used for induction of the renal failure, regardless of the species studied. After ligation of the ureters, lipoprotein concentration increases, but the meaning of this increase for increased serum quinidine binding is not clear.

Acute Kidney Injury↗