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Biomedical subjects

T Jogestrand

Publications and source records attributed to T Jogestrand.

78 records · Page 5Linked to original sources
PubMed1981

Skeletal muscle digoxin concentration during digitalization and during withdrawal of digoxin treatment.

Blood samples and skeletal muscle biopsies (m. quadriceps femoris, vastus lateralis) were taken from 15 patients during digitalization or during withdrawal of digoxin treatment for analysis of serum and skeletal muscle digoxin concentrations. A percutaneous needle biopsy technique was used for muscle sampling and digoxin was analysed by radioimmunoassay. During "slow" digitalization with 0.25 mg digoxin daily the skeletal muscle digoxin concentrations after 2 and 4 days were 45% (range 19%--62%; n = 3) and 78% (range 56%--92%; n= 3) respectively, of the steady state concentration (defined as the digoxin concentration after 25--40 days of treatment). After 9 and 11 days of treatment the skeletal muscle digoxin concentrations were 106% (range 84%--133%; n = 5) and 116% (range 72%--164%; n = 3) respectively, of the steady state concentration. A doubling of the digoxin dose gave a proportional increase in skeletal muscle digoxin concentration (three patients). The magnitude of the estimated half-life of skeletal muscle digoxin was the same as previously reportedly in healthy subjects. No significant correlations were found between changes in systolic time intervals and steady state serum or skeletal muscle digoxin concentrations.

Adult↗
PubMed1981

Effect of digoxin upon intracellular potassium in man.

The effect of digoxin upon intramuscular potassium was studied by use of whole body counting and biopsy technique. Twelve healthy subjects and twelve outpatients with mild cardiac insufficiency or atrial arrhythmia were digitalised. Before and after digitalization total body potassium (TBK) was measured. Potassium concentration in muscle specimens (MK) was analysed by the neutron activation technique. Digoxin was measured in serum and in skeletal muscle tissue by radioimmunoassay, and QS2-index as a measure of the electromechanical systole. In both groups a significant decrease in TBK (P less than 0.05) and MK (P less than 0.01) was demonstrated in connection to digitalization. There was no correlation between the decrease in TBK and MK, or between the concentrations of digoxin in serum or muscle and the decrease in potassium concentration. The digoxin in serum in healthy subjects was 0.9 +/- 0.33 nmol/l and in patients 1.2 +/- 0.41 nmol/l. The digoxin in muscle was 39 +/- 10.9 nmol/kg dry weight in seven of the healthy individuals and 37 +/- 9.5 nmol/kg dry weight in nine patients. After digitalization a decrease of QS2-index was found in both groups (P less than 0.01).

Adult↗
PubMed1980

Digoxin concentration in right atrial myocardium, skeletal muscle and serum in man: influence of atrial rhythm.

Serum, right atrial myocardium and skeletal muscle collected from 32 adult patients undergoing open heart surgery were analyzed for digoxin by radioimmunoassay. Preoperatively 20 patients were in sinus rhythm, but not in patients with atrial fibrillation, there was a highly significant correlation between digoxin concentration in serum and right atrial myocardium, in skeletal muscle and right atrial myocardium, and in serum and skeletal muscle. The means and variances of the ratios right atrial myocardium/serum and right atrial myocardium skeletal muscle were significantly higher in patients with atrial fibrillation than in those with sinus rhythm. This, plus the lack of difference in ratios skeletal muscle serum between these groups of patients, indicate increased right atrial digoxin binding in atrial fibrillation in man. This conclusion is further supported by the finding of similar or higher digoxin concentration in right atrial myocardium than in left ventricular myocardium in atrial fibrillation (6 patients), and a lower digoxin concentration in right atrial myocardium than in left ventricular myocardium in sinus rhythm (3 patients).

Adult↗
PubMed1980

Antiaggregatory, physiological and clinical effects of ticlopidine in subjects with peripheral atherosclerosis.

Twelve patients with varying degrees of peripheral atherosclerotic disease were given an antiaggregatory drug, ticlopidine [5-(6-chlorobenzyl)-4,5,6,7-tetrahydrothieno-(3,2-C)-pyridine HCl] in a single blind trial for one or four months and the effects on platelet aggregation, blood coagulation, marcro- and micro-circulation and walking distance were studied. Two patients were excluded; one because of nausea attributable to the drug, one because of lack of co-operation. No statistically significant changes in circulation parameters or walking distance were noted. No changes were observed in APT-time, thrombine- and Reptilase-clotting time, platelet counts, concentrations of fibrinogen and fibrinopeptide A in plasma or serum antithrombin activity. The mean concentration of fibrinopeptide A was slightly increased in all patients. ADP-induced aggregation was inhibited in all patients. Aggregation induced by arachidonic acid was partially inhibited but not abolished in all patients. Prostaglandin G2-induced aggregation was not altered by ticlopidine but collagen-induced aggregation was inhibited. Ticlopidine, in contrast to acetyl-salicylic acid, inhibits the primary aggregation but also seems to interfere with the release action. Treatment of larger patient groups for longer periods are necessary to determine the clinical usefulness of ticlopidine.

Adenosine Diphosphate↗