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Biomedical subjects

E Karlsson

Publications and source records attributed to E Karlsson.

At least 145 records · Page 8Linked to original sources
PubMed1975

Acetylation of procaine amide in man. A preliminary communication.

The metabolism of procaine amide was studied in 41 cardiac patients who had achieved steady state plasma concentrations of the drug. Acetylated procaine amide accounted for 31 +/- 12% (range 16-63%) of the overall urinary recovery of the drug and is therefore a main metabolite in man. Plasma levels of the metabolite were usually lower but sometimes exceeded those of the parent compound with variations between 1 and 15 mug/ml. The metabolite had a weaker effect than procaine amide on the maximal electrical driving velocity of isolated atrial strips from guinea pig.

Acetylation↗
PubMed1975

Further studies on the binding properties of cobra neurotoxin to cholinergic receptors in mouse skeletal muscle.

Preparations of 3H-monoacetylated derivatives of Naja naja siamensis neurotoxin siamensis 3 were found to be resistant to degradation and deacetylation during in vitro muscle incubation. A low rate of free 3H-acetate (less than 0.4%) was present in the preparations, but should not interfere with the binding of toxin to cholinergic receptors in mouse extensor digitorum longus muscles in vitro. The binding of toxin to cholinergic receptors in mouse extensor digitorum longus muscle was essentially irreversible. d-Tubocurarine antagonized the binding of toxin in both innervated and denervated muscles. Administration of actinomycin D one day after denervation prevented the appearance of new toxin binding sites in the muscles.

Animals↗
PubMed1975

Polymorphic acetylation of procaine amide in healthy subjects.

The acetylation of procaine amide has been studied by means of gas liquid chromatography in 33 healthy human volunteers. The acetylator phenotype was determined by measuring unchanged and acetylated sulphapyridine in urine. Slow acetylators of sulphapyridine excreted significantly less procaine amide in acetylated from in the urine than rapid acetylators (9 plus or minus 1% against 19 plus or minus 4%). Hence, it is suggested that the acetylation of procaine amide is subject to the same genetic polymorphism as that of isoniazid and some sulfonamides.

Acetylation↗
PubMed1975

Procainamide and phenytoin. Comparative study of their antiarrhythmic effects at apparent therapeutic plasma levels.

The antiarrhythmic effects of procainamide and phenytoin were studied in 81 patients admitted to the coronary care unit at the University Hospital in Linköping because of a suspected or proven diagnosis of acute myocardial infarction, and who developed ventricular arrhyhmias, requiring treatment, during the first 8 hours in hospital. Patients were randomly allocated to a procainamide of phenytoin group. The drugs were given as intravenous and oral loading doses followed by oral maintenance therapy. Plasma levels of the two druge were frequently determined and the electrocardiogram was continuously recorded during the 24-hour trial and analysed minute by minute. A significantly higher frequency of therapeutic failure was found in the phenytoin group (23 of 35 patients)compared to the procainamide group(13 of 39 aptients) during the first 2 hours after initiation of therapy. Four patients in the phenytoin group and 2 in the procainamide group developed symptoms probably caused by the trial drugs, necessitating discontinuation of therapy. The mean plasma levels were usually within the apparent therapeutic range (for phenytoin 40-72 mumol/l (10-18 mug/ml), and for procainamide 17-34 mumol/l (4-8 mug/ml). Seventeen patients (68%) in the phenytoin group and 10 patients (48%) in the procainamide group had plasma concentrations within this range when the therapeutic failure was observed. Nine patients died in hospital but only one of them during the trial. The results of this investigation clearly demonstrate the overall superiority of procainamide over phenytoin as an antiarrhythmic drug in short-term therapy after acute myocardial infarction.

Acute Disease↗