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Biomedical subjects

T Jogestrand

Publications and source records attributed to T Jogestrand.

At least 73 records · Page 4Linked to original sources
PubMed1987

Skeletal muscle binding and renal excretion of digoxin in man.

Ten healthy subjects were treated with three or four different doses of digoxin, 0.25 to 0.88 mg daily, in random order. Digoxin concentrations in serum (SDC) and skeletal muscle (SMDC) were determined as well as its renal clearance after 2 weeks of treatment with each dose. The mean ratio SMDC/SDC decreased non-significantly by about 20% from 33 +/- 15 at the lowest SDC interval (0.5-0.9 nmol/l) to 28 +/- 7 at the highest concentration interval (2.0-2.4 nmol/l). This is in accordance with findings from previous studies. No significant change was observed in the renal clearance of digoxin with increasing digoxin concentration, supporting the concept of first-order renal elimination of digoxin.

Adult↗
PubMed1987

Factors limiting physical working capacity in predialytic uraemic patients.

The exercise capacity of 20 predialytic uraemic patients (mean age 43 +/- 12 years) was studied prospectively. Nine of these patients were examined twice in a longitudinal study. The maximal working capacity, measured by standardized exercise test on a bicycle ergometer, averaged 74 +/- 19% of the expected normal. Normal exercise ECG were registered in 16 out of 20 patients. Total hemoglobin/kg body weight (THb) was 67 +/- 16% of the expected normal and serum parathyroid hormone concentration (PTH) was 39 +/- 39 micrograms/l (normal range 0.5-1.5). Partial correlation showed a correlation between exercise capacity and PTH (p less than 0.05). In the longitudinal study the decrease in steady state exercise capacity was correlated to the decrease in THb (p less than 0.05), but not to the increase in PTH. In conclusion, patients with predialytic uraemia have a reduced maximal working capacity, due to several possible factors one of which is a reduced THb. Ischaemic heart disease seems to be of minor importance.

Adult↗
PubMed1986

Effect of digoxin on the electrocardiogram at rest and during exercise in healthy subjects.

The effect of digoxin on the electrocardiogram at rest and during and after exercise was studied in 11 healthy subjects. Exercise was performed on a heart rate-controlled bicycle ergometer with stepwise increased loads up to a heart rate of 170 beats/min. The subjects were studied after peroral intake of digoxin at 2 dose levels and after withdrawal of digoxin. Administration of digoxin induced significant ST-T depression at rest and during exercise even at the small dose (2.4 +/- 0.8 microgram/kg body weight, mean +/- standard deviation). The ST-T changes were numerically small and dose-dependent. The most pronounced ST and T depression occurred at a heart rate of 110 to 130 beats/min. At higher heart rates the ST depression was less pronounced but still statistically significant. During the first minutes after exercise no significant digitalis-induced ST-T depression was seen. This reaction is not of the type usually seen in myocardial ischemia. Fourteen days after withdrawal of the drug there were no significant digitalis-induced ST-T changes at rest or during or after exercise.

Adult↗
PubMed1986

Effects of furosemide and slow-release furosemide on thoracic fluid volumes.

Transthoracic electrical impedance (TEI) was used to assess the relative effectiveness of a 60 mg sustained-release furosemide preparation (FR) and a 40 mg standard furosemide tablet (F), in reducing the fluid content in the thoracic cavity. A double-blind crossover study was performed, in which 12 men with a history of one or more myocardial infarctions and mild left heart failure treated with 40 mg furosemide once daily participated. The trial, lasting 28 days, was divided into two 14-day periods. Each participant received one active drug and one placebo preparation daily, the same regimen being maintained for 14 days, when the active substances were switched. TEI, body weight, serum potassium, sodium, creatinine, and urate were measured immediately prior to the start of the study, after 14 days, and at the end of the study. TEI was measured at frequencies of 1 and 100 kHz with a constant current of 100 microA, during a period of one hour following an intravenous injection of 40 mg furosemide, when the urine volumes were measured also. TEI and urine production after the furosemide injections were similar irrespective of the drug preparation. No evidence of treatment period interaction was seen. No significant differences were demonstrated in body weight and blood chemistry during the trial. These results suggest clinical equipotency of the two preparations in mild left heart failure.

Aged↗
PubMed1986

Beta-blockade and binding of digoxin to skeletal muscle.

The effect of beta-blockade and a 1-h bicycle exercise test on the digoxin concentration in skeletal muscle (thigh) and serum was studied in 10 healthy men, who had ingested 0.5 mg digoxin daily for 2 weeks. Each subject performed two exercise tests at 100-140 W during maintenance digoxin treatment and 24 h after the latest dose. They rested in the supine position for 2.5 h before the exercise. Sixty minutes before the start of the exercise 0.25 mg/kg b.w. propranolol or saline (control) were injected (single-blind). At the end of the exercise the mean heart rate was 30% lower with beta-blockade (P less than 0.001). During exercise the mean skeletal muscle digoxin concentration increased by 29% (P less than 0.01) in the control situation and by 12% (NS) with beta-blockade. The results indicate that propranolol partly inhibits the exercise-induced increase in skeletal muscle digoxin binding. This might be due to inhibition of a catecholamine-induced stimulation of Na+-K+ATPase during exercise.

Adult↗
PubMed1986

Glucose uptake and binding of digoxin to skeletal muscle.

Physical exercise induces increased uptake of both digoxin and glucose in exercising skeletal muscle. Glucose uptake could be a regulatory factor for the digoxin binding to skeletal muscle, since in dogs, insulin and glucose infusion have been reported to increase the uptake of digoxin in muscle. In the present study on eight healthy digitalized subjects (0.5 mg digoxin daily) the uptake of glucose in skeletal muscle was achieved by infusion of 6 mg/kg body weight/min glucose, 0.004 IE/kg body weight/min insulin and 300 micrograms/h somatostatin. Serum and skeletal muscle digoxin levels were analysed before and during the infusion. We found no changes in the digoxin levels in serum and skeletal muscle in spite of an increased uptake of glucose in the muscle. Thus, glucose uptake in skeletal muscle is probably not an important regulatory factor for the change in muscle digoxin binding induced by exercise.

Adult↗
PubMed1985

Treatment of prostatic cancer: effects on serum lipoproteins and the cardiovascular system.

We studied 32 patients with prostatic cancer before, and after 1 and 6 months of treatment with orchiectomy, estramustine phosphate or conventional estrogens (polyestradiol phosphate plus ethinyl estradiol). Lipid metabolism was evaluated by lipoprotein analysis and the intravenous fat tolerance test. Effects on the cardiovascular system were studied by exercise electrocardiography, blood volume estimation and thoracic electrical impedance measurement, a sensitive method to detect early signs of fluid retention. Present treatment programs for prostatic cancer seem to result in effects on lipoprotein metabolism that probably are of minor importance for the development of atherosclerotic manifestations. Measurement of thoracic impedance may be of value to detect fluid retention in individual patients.

Aged↗
PubMed1985

The effect of intravenous prostaglandin E1 on ischaemic pain and on leg blood-flow in subjects with peripheral artery disease: a double-blind controlled study.

The effect of intravenous PGE1 (15 micrograms/h for 72 h) and saline (placebo) on ischaemic resting pains and the macro- and microcirculation was studied in 16 patients with peripheral artery disease. No significant difference in pain relief was observed between PGE1 and placebo. The calf blood-flow was unchanged during both infusions. Skin temperature in the arteriosclerotic foot, however, increased significantly during PGE1 infusion but not during saline infusion. No significant effects were seen on blood-pressure, fluorescein angiography or vital capillary microscopy of the big toe 1 week or 1 month after the PGE1 and placebo infusions.

Aged↗
PubMed1984

Physical exercise and binding of digoxin to skeletal muscle--effect of muscle activation frequency.

Ten healthy subjects who had ingested 0.5 mg digoxin daily for at least 10 days, performed a 1-hour bicycle exercise test on two occasions, 24 h after the latest dose, with the same work load but at two different pedalling rates, 40 and 80 rpm. During exercise the mean digoxin concentration in the thigh muscle increased by 8% at 40 rpm (n.s.) and by 29% at 80 rpm (p less than 0.01). The serum digoxin concentration decreased by 39% at both pedalling rates (p less than 0.001). The results suggest that the increase in skeletal muscle digoxin concentration during exercise is related to the neuromuscular activation frequency. The digoxin concentration in erythrocytes was measured in 16 healthy subjects before and 1 minute after a 1-hour bicycle exercise test. The erythrocyte digoxin concentration decreased by 12% (p less than 0.01) during the exercise indicating that the increased uptake of digoxin in skeletal muscle during exercise influences the digoxin concentration in other tissues.

Adult↗
PubMed1984

Quinidine-induced changes in serum and skeletal muscle digoxin concentration; evidence of saturable binding of digoxin to skeletal muscle.

Eleven patients with atrial fibrillation on maintenance digoxin therapy were investigated by analysis of serum (SDC) and skeletal muscle (SMDC) digoxin concentrations before and 24 h and 2 weeks after starting quinidine treatment. After cardioversion the maintenance dose of digoxin was reduced in order to obtain the same steady-state SDC after 2 weeks, as before quinidine. SDC was increased by quinidine therapy from 1.56 to 2.40 nmol/l after 24 h. With the reduced digoxin dose SDC was 1.68 nmol/l after 2 weeks. The ratio SMDC/SDC decreased after 24 h of quinidine treatment from 35.4 to 29.0 (p less than 0.01). After 2 weeks of quinidine treatment with the reduced digoxin dose, the ratio had risen to 38.1, which did not differ significantly from the initial ratio. The present data suggest that the reduced skeletal muscle binding of digoxin during quinidine therapy is due to saturation of digoxin binding sites secondary to the increase in the total body load of digoxin at steady-state, and not to direct interference by quinidine with digoxin binding sites.

Aged↗
PubMed1983

Cardiac effects of treatment with quinidine and digoxin, alone and in combination.

Systolic time intervals (QS2-I and LVET-I) and echocardiographically determined ejection fraction and velocity of circumferential fiber shortening were recorded in 10 healthy volunteers as measures of inotropic effect during maintenance treatment with 4 consecutive drug regimens: (1) quinidine, 1,200 mg/day; (2) digoxin, average dose 0.31 mg/day; (3) the combination of (1) and (2); and (4) digoxin alone (average dose 0.65 mg/day) to provide the same steady-state serum concentration of digoxin as during the period with combination of digoxin and quinidine. The steady-state serum concentration of digoxin during the low-dose regimen increased from 0.72 +/- 0.15 (mean +/- standard deviation [SD]) to 1.63 +/- 0.28 nmol/liter when quinidine was added. With the high dose of digoxin alone, the serum digoxin level reached 1.68 +/- 0.50 nmol/liter. Skeletal muscle digoxin concentrations during these periods were 27.7 +/- 8.3, 48.7 +/- 16.2, and 51.6 +/- 23.6 nmol/kg of dry weight, respectively. The skeletal muscle to serum concentration ratio of digoxin decreased significantly during quinidine treatment. Systolic time intervals were significantly prolonged by quinidine alone and shortened by digoxin alone, the latter effect being dose-dependent. Subtracting the effect of quinidine itself, the induced increase in digoxin level caused a significant increase in inotropic effect. When these corrected values were compared with those attained during the period with the same steady-state digoxin concentration but in the absence of quinidine, no significant differences were found. Echocardiographically measured ejection fraction and velocity of circumferential fiber shortening showed trends for similar drug effects, as did the systolic time intervals. This study, performed under steady-state conditions, demonstrates that the quinidine-induced increase in steady-state serum digoxin concentration will, with due consideration to quinidine's own pharmacodynamic properties, be accompanied by increased cardiac effects. This indicates that quinidine is not interfering with active receptor sites in the heart for digoxin.

Adult↗
PubMed1983

Physical exercise and digoxin binding to skeletal muscle: relation to exercise intensity.

The effect of a 1 h bicycle exercise test on digoxin concentration in skeletal muscle (thigh) and serum was studied in 10 healthy men, who had ingested digoxin 0.5 mg daily for 2 weeks. During maintenance digoxin treatment each subject performed 2 exercise tests, at 70-90 W and 140-180 W both 24 h after the last dose, at a 2-7 day interval. During exercise at the lower work load the mean skeletal muscle digoxin concentration increased by 9% (n.s.) and the mean serum digoxin concentration decreased by 26% (p less than 0.001). The high work load induced a mean increase in skeletal muscle digoxin of 20% (p less than 0.05) and a mean decrease in serum digoxin of 40% (p less than 0.001). The results indicate that the increased uptake of digoxin into exercised skeletal muscle and the decrease in serum digoxin during exercise is related to the intensity of the exercise.

Adult↗
PubMed1983

Serum digoxin determination in outpatients--need for standardization.

1 Blood samples were taken from 30 outpatients for serum digoxin analysis before and after 5 min-4 h of rest in the supine position. 2 The digoxin concentration increased significantly during rest and a steady-state concentration was reached after approximately 2 h of rest. 3 The mean increase in serum digoxin after 2 h of rest was 23% with a considerable range, i.e. 0-75% (0-0.6 nmol/l). 4 On the analogy of a previous finding of a decrease in serum digoxin concentration during exercise in healthy subjects ingesting digoxin, the present results suggest that everyday physical activity affects the serum digoxin concentration. Standardized rest in the supine position prior to collecting blood samples from outpatients is therefore necessary for reliable serum digoxin determinations.

Aged↗
PubMed1983

Skeletal muscle digoxin binding in patients with renal failure.

For digoxin analyses blood and skeletal muscle samples were taken from seven digoxin-treated patients with chronic renal failure. The ratio between skeletal muscle and serum digoxin concentration in the patients with renal failure was not significantly different from the ratios in two control groups consisting of subjects with normal renal function. In the group of patients with renal failure there was no relationship between the glomerular filtration rate and muscle digoxin binding (specific plus unspecific). The present study does not indicate reduced skeletal muscle digoxin binding in patients with chronic renal failure.

Adult↗
PubMed1983

Effect of digoxin on physical performance in healthy man.

The effect of digoxin on the maximal oxygen uptake, the heart rate reaction during submaximal and maximal bicycle exercise and the isokinetic skeletal muscle strength in the thigh was investigated in nine well-trained healthy young men. A daily dose of digoxin of 0.50 mg for 2 weeks, giving a steady state serum digoxin concentration of 1.0 +/- 0.2 nmol/l, did not significantly change maximal oxygen uptake or isokinetic muscle strength. However, the heart rate at rest and during exercise, both at submaximal and maximal levels, decreased significantly during digoxin administration.

Administration, Oral↗
PubMed1983

Estimation of digital circulation and its correlation to clinical signs of ischaemia--a comparative methodological study.

Five different methods were used to evaluate the arterial blood supply to 29 toes from 15 patients with atherosclerotic disease: digital pulse plethysmography, systolic toe blood pressure recording, skin temperature recording, vital capillary microscopy and dynamic fluorescein angiography. An optimal discrimination between legs with and without ischaemic ulcers or gangrene was obtained with the following borderlines: inclination time non-measurable because of very low or no recordable pulse curve, systolic toe blood pressure less than 20 mmHg, skin temperature (after vasodilatation) less than 29 degrees C, capillary stage greater than 3 (indicating the presence of capillary haemorrhages or more advanced changes) and fluorescein appearance time greater than 45 s. The results of the study provide no basis for the opinion that one method is superior to the others in discriminating between arteriosclerotic feet with and without existing skin necrosis.

Aged↗
PubMed1981

Skeletal muscle digoxin concentration and its relation to serum digoxin concentration and cardiac effect in healthy man.

Blood samples and skeletal muscle biopsies (m. quadriceps femoris, vastus lateralis) were taken from seven healthy subjects for analysis of serum and skeletal muscle digoxin concentrations by radioimmunoassay using a percutaneous needle biopsy technique for muscle sampling. The subjects were investigated on two digoxin dose levels and on the third day after withdrawal of digoxin. It was found that the skeletal muscle/serum digoxin ratio was significantly higher than the corresponding ratio obtained in a previous study with muscle sampling (m. rectus abdominis) from patients during open heart surgery. The present study indicates a significant correlation between the digoxin concentrations in serum and skeletal muscle as well as between cardiac effect, measured by changes in QS2I, and skeletal muscle digoxin concentration. A doubling of the digoxin dose gave a proportional increase in skeletal muscle digoxin concentration. The magnitude of the estimated half-life of skeletal muscle digoxin was the same as previously reported for serum or plasma digoxin.

Adult↗