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Biomedical subjects

R F Maronde

Publications and source records attributed to R F Maronde.

At least 37 records · Page 2Linked to original sources
PubMed1979

Pharmacokinetics, pharmacology of atenolol and effect of renal disease.

1. The pharmacokinetics of intravenous and oral atenolol (50 mg) in six healthy volunteers was studied. Plasma, saliva and urine were collected up to 24 h after each dose. 2. There was no significant difference in atenolol half-life when administered by the two routes. Bioavailability of the orally administered atenolol was 50%. 3. Atenolol levels in saliva required about 2 h to reach equilibrium with plasma drug levels. 4. A comparison between the pharmacokinetics and pharmacology of atenolol was made in twelve healthy subjects. 5. Dose-independent pharmacokinetics were observed. Reductions in resting heart rate and arterial blood pressure were proportional to either the logarithm of dose or area under the plasma concentration time curve or cumulative urinary atenolol excretion. 6. Plasma elimination half-life in five subjects with renal failure was prolonged.

Administration, Oral↗
PubMed1978

GLC determination of atenolol and beta-blocking agents in biological fluids.

A rapid, sensitive, and specific method of analysis for atenolol is described. Metoprolol is used as the internal standard. Atenolol and metoprolol are extracted into 1-butanol--benzene. Interfering components present in palsma and urine, but not discolored saliva, are removed during an acid wash and reextraction into ether. Drug and internal standard are converted to the pentafluoropropionate derivatives, which are quantitated by GLC with electron-capture detection and characterized by chemical-ionization mass spectrometry. The method should be applicable to measurement of other beta-adrenergic blocking agents with similar structures.

Adrenergic beta-Antagonists↗
PubMed1976

Rapid GLC determination of fusaric acid in biological fluids.

A simple, sensitive GLC assay was developed for fusaric acid, the active metabolite of bupicomide, to follow the disposition of this investigational antihypertensive agent in patients undergoing therapy. Fusaric acid is efficiently extracted from biological samples, derivatized by on-column methylation, and chromatographed using flame-ionization detection. An internal standard is utilized to quantitate results. The procedure is rapid and specific for fusaric acid, and has a lower limit of sensitivity of 0.1 mug/ml. The method is suitable for supporting pharmacokinetic studies of bupicomide following therapeutic doses in animals and humans.

Body Fluids↗
PubMed1972

Prescription data processing--its role in the control of drug abuse.

Prescriptions in an outpatient setting were kept on file for immediate recall by computer terminals. Drugs with abuse potential were found to make up 33.6 percent of all prescriptions, and 12.4 percent of these prescriptions were for excessive quantities. An additional 2.6 percent of these prescriptions represented irrationally large quantities of drugs dispensed by multiple prescriptions. The physician was cooperative and willing to correct this situation when it was brought to his attention by the pharmacist.

California↗
PubMedDate not supplied

Effect of probenecid on the natriuresis and renin release induced by bumetanide in man.

In a randomized crossover trial in six normal male subjects, the effect of pretreatment with probenecid on natriuresis and renin release in response to bumetanide was studied. The subjects received 120 mEq sodium and 80 mEq potassium per day. A single dose of 2 mg bumetanide was administered on the fourth morning after pretreatment with either placebo or probenecid. Creatinine and uric acid were measured in serum and urine, plasma renin activity was determined by radioimmunoassay of angiotensin I, and plasma and urine concentrations of bumetanide were measured by a highly sensitive radioimmunoassay method. Probenecid reduced both natriuresis and hyperreninemia induced by bumetanide. This effect is postulated to be due not to a direct action on sodium excretion but is probably secondary to inhibition of renal tubular secretion of bumetanide. Consequently, these findings appear to support the concept that the quantity of bumetanide delivered to the tubular lumen is an important determinant of its diuretic effect.

Adult↗
PubMedDate not supplied

Sympathetic system function and vascular reactivity in hypercalcemic patients.

To elucidate the pathophysiology of elevated blood pressure in hypercalcemic patients, we studied the plasma concentration of catecholamines and their major metabolites (as an index of sympathetic function) and the blood pressure response to norepinephrine infusion (vascular reactivity) in patients with primary hyperparathyroidism, in patients with primary hypertension, and in normal controls. In addition, we evaluated the hemodynamic response to calcium infusion in normotensive and hypertensive subjects. Plasma levels of both norepinephrine and epinephrine and the metabolites normetanephrine and dihydroxyphenyl-glycol were significantly higher in the hypercalcemic group than in the other two groups. Norepinephrine infusion increased blood pressure by 8.5 +/- 1.4 mm Hg in the control group, by 19 +/- 2 mm Hg in the hypercalcemic group and by 29 +/- 3 mm Hg in the primary hypertensive group. Infusion of calcium produced a significant rise in both systolic and diastolic blood pressures and in peripheral resistance in the hypertensives, whereas in the normotensive group only systolic blood pressure increased, associated with a rise in cardiac output. We conclude that the observed increased activity of the sympathetic nervous system in hypercalcemia could account for the elevation in blood pressure and the enhanced vascular reactivity could explain the hypertension in some patients with primary hyperparathyroidism.

Adult↗