PubMed Health⌕ Search

Biomedical subjects

A Nørgaard

Publications and source records attributed to A Nørgaard.

At least 37 records · Page 2Linked to original sources
PubMed1994

Exercise capacity in patients with left ventricular dysfunction following acute myocardial infarction: relation to systolic and diastolic function and intervention with captopril.

Patients with acute or chronic heart disease may have limited exercise capacity if they have reduced left ventricular function. Indexes of reduced left ventricular function during exercise are a predictor of subsequent survival although left ventricular ejection fraction is a poor predictor of physical endurance. We evaluated the effect of captopril on physical endurance in 48 males with left ventricular dysfunction following myocardial infarction. On the 7th day following myocardial infarction patients were randomized to either captopril 50 mg daily or corresponding placebo. Patients were followed up by means of serial echocardiography and exercise stress testing for a period of 180 days. Exercise capacity was significantly improved in the captopril group. Changes in exercise capacity were significantly correlated to changes in left ventricular (LV) volumes and compliance. The beneficial effect of captopril on exercise capacity was probably mediated via improvement in LV performance and compliance.

Captopril↗
PubMed1994

Ventricular arrhythmias in the acute and chronic phases after acute myocardial infarction. Effect of intervention with captopril.

BACKGROUND: Ventricular arrhythmias (VAs) are independent predictors of mortality in survivors of myocardial infarction (MI), and they are more likely to be induced in dilated hearts with increased wall stress. Angiotensin-converting enzyme (ACE) inhibitors have been shown to prevent progressive dilation of the left ventricle after MI. METHODS AND RESULTS: The effects of captopril were evaluated in 58 patients with left ventricular (LV) dysfunction after MI. Patients were randomized on day 7 to either placebo or captopril (50 mg daily) in a double-blind parallel study over a period of 6 months. Patients were followed up by means of ambulatory ECG monitoring and echocardiography. There was a significant increase in VA in the placebo group (P < .05) in contrast to a significant decrease in the captopril group (P < .05). As a consequence, there was a significant between-group difference after 6 months (P < .05). Furthermore, the number of patients without VA at baseline who presented with this at the completion of the study was 6% in the captopril group versus 38% in the placebo group (P < .05). At baseline as well as at the termination of the study, LV end-diastolic volume index (LVEDVI) and LV end-systolic volume index (LVESVI) were significantly increased among patients with VA (P < .01). On day 180, both myocardial ischemia and an increase in the LVEDVI were independent predictors of VA; however, progressive dilation of the left ventricle was confined to the placebo patients with significant increases in the LVEDVI compared with the captopril group: 17% versus 0%, respectively (P < .01). Furthermore, the duration of ambulatory ST-segment depression was significantly longer in this group compared with the captopril group (P < .01). CONCLUSIONS: Dilation of the left ventricle and myocardial ischemia predict VA during both the acute and chronic phases after MI. In post-MI patients with LV dysfunction, captopril has a beneficial effect on both the number of complex VAs as well as the number of patients who develop VA during the chronic phase. This is in all probability mediated through effects on both LV remodeling, LV function, and myocardial ischemia in patients who are exposed to an increased risk of undergoing progressive dilation of the left ventricle.

Acute Disease↗
PubMed1993

Activation of human phagocytes by Helicobacter pylori. A novel interaction with neutrophils and monocytes distinct from that of N-formylated oligopeptides.

Sonicate proteins from Helicobacter pylori activate human neutrophils and monocytes for chemotactic and oxidative burst responses. The molecular nature of this activity and its interaction with the phagocyte membrane is unknown. Cross-stimulation experiments were performed with human neutrophils and monocytes preincubated in H. pylori sonicate and subsequently stimulated with the established and characterised stimuli N-f-methionyl-leucyl-phenylalanine (fMLP), the complement split product C5a (in zymosan-activated serum, ZAS), and phorbol-myristate-acetate (PMA). Checkerboard experiments confirmed the sonicate to be truly chemotactic, whereas no chemokinetic activity was demonstrated. At high concentrations of sonicate (1 mg/ml), a depressed chemotactic and oxidative burst response was observed, whereas the viability was > 98%. At lower concentrations (0.01-0.1 mg/ml), only weak deactivation could be induced for monocytes, i.e. the cells had a normal function. With neutrophils, even low concentrations of sonicate depressed the oxidative burs responsiveness. However, the reduced activity was unrelated to the stimulus applied indicating that H. pylori protein(s) activate human neutrophils and monocytes by a membrane binding site distinct from that of previously described receptors.

Chemotaxis, Leukocyte↗
PubMed1992

Enalapril and exercise-induced hyperkalemia. A study of patients randomized to double-blind treatment with enalapril or placebo after acute myocardial infarction.

During exercise a marked increase in plasma potassium in healthy subjects has repeatedly been demonstrated. In patients on treatment with angiotensin-converting enzyme inhibitors this may be further augmented. Therefore, the aim of present study was to evaluate the effect of enalapril on exercise-induced hyperkalemia. This was done in patients with acute myocardial infarction randomized to double-blind treatment with enalapril 10-20 mg per day (n = 7) or placebo (n = 6) within 24 h of onset of chest pain, and the results were compared with data from healthy control subjects (n = 11). Baseline plasma potassium did not differ between the three groups; i.e. 4.2, 4.0, and 4.1 mmol/l, respectively. An incremental, symptom-limited, bicycle exercise test was done one month after the myocardial infarction, and blood samples were taken for determination of plasma potassium. The exercise-induced increase in plasma potassium was not higher in the enalapril group as compared to the placebo and control groups, and there was no difference between the enalapril and placebo group, the specific values being 0.6 vs. 0.6 and 0.7 mmol/l, respectively. No difference was observed in the slope (dK/dt) between the 3 groups. In conclusion, enalapril at a dosage of 10-20 mg per day does not provoke any augmentation of the increase in plasma potassium during exercise.

Adult↗
PubMed1992

Egg and milk allergy in adults. Diagnosis and characterization.

Nineteen adult patients representing a total of 24 medical histories of immediate adverse reactions to egg or cows' milk underwent 1) standardized questioning about signs/symptoms occurring less than 2 h after ingestion of egg or milk, 2) skin prick test, RAST and histamine release test, and 3) titrated, oral, double-blind, placebo-controlled challenge (DBPCFC) with fresh egg or milk. Eleven medical histories (46%) were confirmed by DBPCFC in 10 patients (53%). All DBPCFC-positive patients experienced gastrointestinal symptoms, and in 80% of the patients, gastrointestinal symptoms were accompanied by respiratory or skin symptoms. Threshold doses varied between 50 mg and 250 g, with 4 patients presenting objective signs following 5 g or less. DBPCFC-positive patients reported significantly more symptoms and had a significantly higher number of positive tests than had DBPCFC-negative patients. None of the tests were in significant concordance with DBPCFC, although RAST showed a sensitivity of 100%. Thus, DBPCFC cannot be substituted in the diagnosis of milk and egg allergy in adults. The use of titrated, fresh foods in DBPCFC proved to be a safe and well-controlled procedure.

Adolescent↗
PubMed1991

Digitalis enhances exercise-induced hyperkalaemia.

In 9 patients with atrial fibrillation the effect of zero, low and high levels of serum digoxin on exercise-induced hyperkalemia was assessed by bicycle exercise tests. Exercise at each level of serum digoxin was associated with a significant (up to 20%) rise in plasma potassium. At a work load of 75 W the highest level of serum digoxin was associated with a significantly higher maximum plasma potassium concentration as compared to the maximum valueatazero serum digoxin. The enhancement of exercise-induced hyperkalemia may add to the arrhythmogenic effect of digitalis.

Adult↗
PubMed1990

Effect of amiodarone on 3H-ouabain binding sites in human skeletal muscle.

Na,K-ATPase, or the Na,K-pump, is essential for the excitability and contractility of muscle tissue. Hypothyroidism in associated with a marked decrease in the Na,K-pump concentration in skeletal muscle and myocardium. In 7 patients on long-term amiodarone treatment there was a 36% reduction in the concentration of 3H-ouabain binding sites in skeletal muscle biopsies compared to 7 healthy subjects. This decrease during long-term amiodarone treatment may represent an equivalent reduction in the concentration of the functional Na,K-pump and it may be important in the adverse effect of amiodarone on muscle.

Adult↗
PubMed1990

The concentration of the Na,K-pump in skeletal and heart muscle in congestive heart failure.

Na,K-ATPase (or the Na,K-pump) is essential for excitability and contractility of muscle tissue. Previous studies have shown a decrease in the concentration of this pump in endomyocardial biopsies from patients with dilated cardiomyopathy. The effect of congestive heart failure on the concentration of Na,K-ATPase in skeletal muscle was assessed in 16 patients by measurement of binding of 3H-ouabain to biopsies of the vastus lateralis muscle. Ten patients had impaired left ventricular function with an ejection fraction of 0.32 +/- 0.03 and a concentration of the Na,K-pump of 229 +/- 15 pmol/g wet weight in the skeletal muscle, whereas 6 patients had an ejection fraction of 0.66 +/- 0.05 (P less than 0.001) and a concentration of 307 +/- 17 pmol/g wet weight (P less than 0.01). In endomyocardial biopsies, the concentration of Na,K-ATPase was 340 +/- 37 and 500 +/- 39 pmol/g wet weight (P less than 0.025) in patients with impaired and normal ventricular function, respectively. There was a significant correlation between the concentration of the Na,K-pump in the biopsies of the skeletal muscle and ejection fraction, as well as between its concentration in the endomyocardial and skeletal muscular biopsies (r = 0.56, P less than 0.025 and r = 0.72, P less than 0.005, respectively). The decrease in concentration of the pump in skeletal muscle may contribute to the limitation of exercise capacity in congestive heart failure.

Adult↗
PubMed1990

Human skeletal muscle Na, K-ATPase concentration quantified by 3H-ouabain binding to intact biopsies before and after moderate physical conditioning.

The putative effect of moderate training on human skeletal muscle Na,K-ATPase concentration and thus on the capacity for active uptake of potassium was evaluated. In 15 conscripts the Na,K-pump concentration was determined in vastus lateralis muscle by measurement of 3H-ouabain binding to intact muscle biopsies before and after 10 weeks of physical training. All subjects had improved physical fitness, body weight was reduced by 3% (P less than 0.001), Cooper's test showed an improvement by 7% (P less than 0.05) and leg circumference 10 cm above the knee joint had increased by 3% (P less than 0.001). Mean Na,K-pump concentration +/- S.E.M. in vastus lateralis muscles was 308 +/- 13 (N = 15) and 300 +/- 7 (N = 15) pmol x g wet wt.-1 (P less than 0.60) before and after training, respectively. Thus, in human subjects moderate improvement of physical performance may occur without any change in skeletal muscle Na,K-pump concentration. It may be, however, that change in the acute regulation of skeletal muscle Na,K-ATPase--i.e. augmented activity of existing Na,K-pumps--may reduce exercise-induced rise in plasma potassium concentration after moderate physical conditioning. Since the circumference of the legs had increased, the total amount of Na,K-ATPase in the legs had probably increased. Hence, moderate training may induce muscle hypertrophy with a balanced synthesis of muscle mass and Na,K-pumps.

Adolescent↗
PubMed1990

Exercise-induced hyperkalaemia can be reduced in human subjects by moderate training without change in skeletal muscle Na,K-ATPase concentration.

In 15 conscripts, venous plasma potassium was followed during exercise on a training bicycle before and after 10 weeks of moderate physical training and a putative relationship with skeletal muscle Na,K-ATPase was evaluated. Peak plasma potassium concentration obtained at exhaustion was 6.1 +/- 0.2 and 5.6 +/- 0.2 mmol l-1 (mean +/- SEM, n = 14, P less than 0.05) before and after training, respectively. Throughout the exercise period and within the first minutes of rest plasma potassium concentration was 0.2-0.5 mmol l-1 higher before than after training. Neither peak values nor peak rises in plasma potassium concentration before nor after training were correlated to the 3H-ouabain binding site (Na,K-ATPase) concentration in vastus lateralis muscle. The results indicate that net loss of potassium from the skeletal muscle pool during exercise is reduced after training, that the heart during exercise may be exposed to a smaller rise in plasma potassium concentration after training than before, and that moderate improvement of capacity to clear extracellular potassium during exercise may be due to increased activity of existing Na,K-pumps in resting skeletal muscle fibres. This may reduce muscle fatigue, increase physical performance and explain the paradoxical observation that, despite an increased catecholamine response, there is a reduced risk of cardiac events after training.

Adolescent↗
PubMed1988

Relation of left ventricular function and Na,K-pump concentration in suspected idiopathic dilated cardiomyopathy.

The possible relation between Na-K-pump concentration and left ventricular (LV) function was studied in 24 patients with suspected idiopathic dilated cardiomyopathy. This was done by measurement of 3H-ouabain binding to biopsies obtained during left-sided heart catheterization. In all patients light microscopy of biopsies was compatilel with dilated cardiomyopathy. Nineteen patients had impaired LV function as defined by NYHA/WHO and a Na,K-pump concentration of 331 +/- 19 pmol/g wet weight, whereas 5 patients had normal LV function and a Na,K-pump concentration of 559 +/- 62 pmol/g wet weight (p less than 0.001). The correlation between Na,K-pump concentration and ejection fraction was highly significant n = 24, r = 0.81, p less than 0.001). There was no correlation between volume fraction of collagen tissue and Na,K-pump concentration in the biopsies (n = 24, r = -0.08, p less than 0.80), indicating that the decrease in Na,K-pump concentration with dilated cardiomyopathy is not the simple outcome of increased fibrosis in the myocardium. The results indicate that the decrease in Na,K-pump concentration may be of importance for myocardial dysfunction and suggest a simple biochemical assessment of dilated cardiomyopathy by measurement of 3H-ouabain binding.

Adult↗
PubMed1988

Na+,K+-ATPase concentration in rodent and human heart and skeletal muscle: apparent relation to muscle performance.

To investigate whether the sodium-potassium pump or Na+,K+-ATPase concentration in muscles is related to the capacity for muscle performance, the 3H-ouabain binding site concentration or 3-O-methylflourescein phosphatase activity was determined in samples of heart ventricular muscles from trained rats, cardiomyopathic hamsters, and human subjects. These methods have earlier been shown to quantify the Na+,K+-ATPase concentration in muscle tissue with high accuracy. When rats were swim trained for six weeks the heart ventricular muscle Na+,K+-ATPase concentration was increased by 20% (p less than 0.02) and the heart to body weight ratio by 14% (p less than 0.005). The increase in Na+,K+-ATPase concentration was only slowly reversible. After three weeks of deconditioning an increase of 12% (p less than 0.05) was still observed. In comparison skeletal muscle Na+,K+-ATPase concentration was increased by up to 46% (p less than 0.001) and decreased by up to 30% (p less than 0.005) after training and immobilisation respectively. Cardiomyopathic hamsters showed a reduction of 33% (p less than 0.005) in the heart ventricular Na+,K+-ATPase concentration compared with normal hamsters. This decrease was associated with a heart to body weight increase of 19% (p less than 0.01) and congestive heart failure. In six patients with a mean ventricular ejection fraction of 68% the mean Na+,K+-ATPase concentration in endomyocardial biopsy specimens obtained by left heart catheterisation was 505(41) compared with 322(32) pmol.g-1 wet wt (p less than 0.001) in nine patients with a mean ejection fraction of 29%. Taken together the present data indicate a relation between the Na+,K+-ATPase concentration and the capacity for muscle performance.

Animals↗
PubMed1987

Quantification of rat sciatic nerve (Na+,K+)-ATPase by measurements of [3H]ouabain binding in intact nerve samples.

The (Na+,K+)-ATPase concentration in rat sciatic nerve was quantified by measurements of [3H]ouabain binding to intact nerve samples in a vanadate-Tris buffer. This gave values of 145-172 pmol/g wet weight in mature female rats. The methodological errors of the [3H]ouabain binding assay was identified, quantified and corrected for. The [3H]ouabain binding sites were homogeneous with respect to [3H]ouabain affinity with an apparent dissociation constant of 5 X 10(-8) mol/l, i.e. in the same range as in samples of skeletal muscles incubated at similar conditions. Post-mortem the [3H]ouabain binding site capacity in rat sciatic nerve decreased with a half-life time of 5 days, allowing measurements to be performed within 6 h after death with a reduction in [3H]ouabain binding sites of only 3%. When nerve samples were frozen the [3H]ouabain binding site concentration remained constant. An increase in sciatic nerve [3H]ouabain binding site concentration of 122% was seen from the 2nd to the 4th week of life followed by a decrease of 53% to the 12th week of life. In mature males the [3H]ouabain binding site concentration was 1.8 times that in nerves from age-matched female rats. Denervation caused a reduction of 61%, whereas K+ depletion or thyroid status has no effect on sciatic nerve [3H]ouabain binding site concentration.

Age Factors↗