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Biomedical subjects

B Beermann

Publications and source records attributed to B Beermann.

At least 91 records · Page 5Linked to original sources
PubMed1978

Placental transfer of furosemide.

After oral administration of furosemide to 18 pregnant women on the day of delivery, substantial concentrations of the drug were detected in umbilical cord vein plasma as well as in amniotic fluid. The ratio between the furosemide concentrations in maternal vein plasma and in umbilical cord plasma increased with time and approximated unity at 8 to 10 hr after administration of the drug. The plasma half-life of furosemide appeared to be longer in the mothers than in nonpregnant healthy volunteers. In one patient the plasma level of furosemide was constant during 5 hr of observation.

Amniotic Fluid↗
PubMed1978

Effect of food on the bioavailability of bendroflumethiazide.

Bendroflumethiazide (BFT), 10 mg, was given orally to eight subjects after fasting overnight and together with a meal. Concentrations of the diuretic in plasma and urine were determined by GLC. As judged by AUC and urinary recovery of BFT, the bioavailability of the diuretic was not influenced by concomitant intake of a meal.

Administration, Oral↗
PubMed1977

Bioavailability of two hydrochlorothiazide preparations.

Eight healthy volunteers received hydro-chlorothiazide 75 mg as Dichlotride and Esiderx. Maximal plasma levels were significantly (p less than 0.05) higher after Dichlotride than Esidrex, 512 +- 189 and 376 +- 70ng/ml, respectively. However, the bioavailability of the two brands of hydrochlorothiazide did not differ significantly as judged by comparison of the AUC0 leads to 9h and AUC0 leads to chi, and the urinary recovery of hydrochlorothiazide during 48 hrs.

Adolescent↗
PubMed1977

Elimination of furosemide in healthy subjects and in those with renal failure.

Furosemide was administered intravenously to 5 healthy volunteers and 15 patients with various degrees of renal failure. Two patients were given the drug orally. The plasma half-life of furosemide averaged 0.79 hr in the healthy subjects. Although most patients with kidney disease had a prolonged half-life (t1/2), up to 24.58 hr, some with advanced renal failure had an almost normal t1/2. The plasma clearance of furosemide, which in the normal subjects averaged 194 ml/min, decreased proportionally with decreasing creatinine clearance, as did the renal clearance, which in the healthy subjects averaged 95 ml/min. There was no correlation between kidney function and the apparent volume of distribution or of nonrenal clearance. One patient was given 35S-labeled furosemide intravenously. Although the furosemide plasma t1/2 was essentially normal, the elimination rate of metabolites was decreased. Unlike that of healthy subjects, the main route of excretion of label was in the feces.

Administration, Oral↗
PubMed1977

Pharmacokinetics of bendroflumethiazide.

Bendroflumethiazide (bft), 10 mg, was administered orally to 9 healthy volunteers. The concentrations of the diuretic in plasma and urine were determined by gas-liquid chromatography (GLC). Peak plasma levels (86 +/- 18 ng/ml) of bft were reached at 2 +/- 0.4 hr. The concentration declined with a mean t1/2 of 3.0 hr. The apparent volume of distribution averaged 1.48 L/kg. The major part of the drug was eliminated via nonrenal mechanisms, the nonrenal clearance being estimated to 269 +/- 77 ml/min and renal clearance to 105 +/- 24 ml/min. Urinary recovery of the thiazide averaged 30%.

Adolescent↗
PubMed1976

Absorption, metabolism, and excretion of hydrochlorothiazide.

14C-hydrochlorothiazide (hct) was administered orally (n=4) and iv (n = 2 to healthy subjects. The gastrointestinal absorption ranged between 60% and 80%, most of it took place in the duodenum and the upper jejunum. The radioactivity was eliminated mainly in the urine, while no sigificant biliary excretion was observed. Chromatographic analysis of the urinary radioactivity demonstrated that greater than 95% of the absorbed or injected 14C-hct was excreted unchanged. The radioactivity in plasma during the first 10 hr after oral administration declined with a fast phase but the levels of label thereafter suggested a slow phase. The existence of such a phase was verified in 1 subject given 75 mg hct orally. His plasma levels of hct (determined with gas-liquid chromatography) declined according to a 2-compartment model, the half-lives of the alpha-and beta-phases being 1.7 and 13.1 hr, respectively. Hct accumulated in the blood cells and the ratio between the radioactivity in cells and that in plasma averaged 3.5. The fate of a single dose of 14C-hct in 2 hypertensive patients treated with the drug chronically was similar to that in the healthy subjects. A third patient, who had slightly elevated serum creatinine, eliminated hct more slowly than the others. Like the healthy subjects, the patients eliminated hct to greater than 95% in unchanged form.

Adult↗
PubMed1975

On the fate of furosemide in man.

35S-furosemide was administered orally (n=7) or i.v. (n=2) to healthy subjects. The average gastrointestinal uptake estimated by comparison of the urinary recovery of label and the areas under the plasma curves after the two routes of administration was 65%. The half life of radioactivity in the plasma after oral 35S-furosemide was 90 +/- 17 min (estimated on the slope between 2 and 6 h); the corresponding figure after 35S-furosemide i.v. was 47-53 min (slope 0.5-4 h). There was probably a slower phase after 4-6 h. Fractionation of labelled material in urine from two subjects demonstrated that approximately two thirds of the label recovered at 24 h had the same chromatographic properties as furosemide. A major part of the metabolite(s) was probably furosemide glucuronide. There was no evidence that 4-chloro-5-sulfamoylanthranilic acid was formed in man. The total urinary recovery of label (5-7 d) after oral and intravenous administration was 55.1 +/- 3.2 (mean +/- SD) and 82-84%, respectively. After 35S-furosemide i.v., 6-9% of the label was recovered in faeces, and it could not be accounted for solely by biliary excretion of furosemide.

Administration, Oral↗
PubMed1975

Binding-site interaction of chlorthalidone and acetazolamide, two drugs transported by red blood cells.

When 14C-chlorthalidone was administered orally to 2 healthy volunteers, the total recovery of radioactivity in urine (about 75 percent) and feces was close to 100 percent. Most of the label recovered in the blood was bound to the blood cells. When the procedure was repeated while the 2 subjects were receiving acetazolamide, the excretion of labeled material in urine and feces was essentially unchanged, but the blood cells contained less and the plasma more of the blood radioactivity. The half-life of the radioactivity in plasma and blood cells had decreased by about 65 percent. Intravenous administration of acetazolamide (single dose) to 2 other subjects who had received 14C-chlorthalidone orally resulted in a marked drop in the blood cell radioactivity, whereas that in plasma increased. The affinity of chlorthalidone for red blood cells was further evidenced on incubation of 14C-chlorthalidone with human blood. Of the incubated radioactivity, 94 percent to 99 percent was recovered in the erythrocytes. Preincubation of the blood samples with acetazolamide prior to the addition of 14C-chlorthalidone, as well as incubation of acetozolamide in blood samples previously incubated with 14C-chlorthalidone, demonstrated that acetazolamide is able to inhibit and to displace chlorthalidone from blood cells. There are several lines of evidence indicating that chlorthalidone is transported attached to the erythrocyte carbonic anhydrase.

Acetazolamide↗
PubMed1975

Advanced heart block aggravated by carbamazepine.

This report presents a serious adverse reaction to the anticonvulsant compound carbamazepine. A woman was admitted to hospital for recurrent attacks of syncope. She suffered from atrioventricular block of the Mobitz type II. Carbamazepine suppressed the conduction in her already defective Purkinje fibres and induced ventricular stand-still with subsequent Adams-Stokes attacks.

Adams-Stokes Syndrome↗