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Biomedical subjects

L Gullestad

Publications and source records attributed to L Gullestad.

At least 19 recordsLinked to original sources
PubMed1992

[Sudden cardiac death. Significance of beta blockaders].

Sudden death accounts for about 15-20% of all natural fatalities in the industrially developed world. Most of the victims have a substrate of extensive myocardial injury caused by coronary heart disease, cardiomyopathy and hypertensive heart disease. In most cases, the immediate cause of death is triggered by ventricular tachycardia which degenerates into ventricular fibrillation. Changes in myocardial electrical properties may be critically modified by ischemia, imbalance in the autonomic nervous system, electrolytic disorders, and haemodynamic factors. We review the causes of sudden cardiac death, giving special attention to the effect of beta-adrenoceptor blockade as a preventive measure.

Adrenergic beta-Antagonists↗
PubMed1992

[Myocardial disease in diabetes mellitus].

Diabetes mellitus is associated with excessive cardiovascular morbidity and mortality. Patients with diabetes mellitus suffer premature and severe atherosclerosis, and the relative impact is greater in women than in men. Clinical, experimental and pathological studies support the existence of a specific cardiomyopathy associated with diabetes mellitus. The cardiomyopathy plays an essential role in the pathogenesis of primary myocardial involvement, resulting in ventricular dysfunction, diminished cardiac pump performance and eventually overt heart failure. The authors discuss coronary heart disease and diabetic cardiomyopathy and indicate relevant treatment regimens.

Cardiomyopathies↗
PubMed1992

Differential effect of selective beta 1 and nonselective beta-adrenoceptor blockade on epinephrine and atropine response in normal humans.

Sympathetic stimulation with epinephrine (EPI) combined with parasympathetic blockade with atropine was studied in 10 healthy volunteers premedicated with placebo or three different beta-adrenoceptor blockers: atenolol (62.5 micrograms/kg, beta 1-selective), propranolol (62.5 micrograms/kg, nonselective), and pindolol (7.5 micrograms/kg, nonselective with intrinsic sympathomimetic activity, ISA). EPI infusion (0.06 microgram/kg/min) after placebo increased heart rate (HR) and systolic blood pressure (SBP) and decreased diastolic BP (DBP). Pretreatment with atenolol reduced the HR increase, and caused similar changes in BP. In contrast, pretreatment with propranolol and pindolol decreased HR and increased BP. Combined EPI and atropine (15 micrograms/kg) after placebo increased HR by 40% without causing BP changes. Similar HR changes were observed after administration of all beta-adrenoceptor blockers, but whereas a marked pressor response was observed after propranolol and pindolol a blunted response was observed after atenolol. Propranolol and pindolol reduced myocardial oxygen demand estimated by the HR x BP product after EPI, but this response was abolished by atropine. Serum potassium decreased from 3.9 +/- 0.2 to 3.2 +/- 0.3 mM after EPi and atropine. This effect was less after atenolol, and potassium increased after premedication with propranolol and pindolol. Our results show that nonselective beta-adrenoceptor blockade has a favorable effect on potassium homeostasis and oxygen demand parameters during EPI infusion but causes a marked pressor response, contrary to a beta 1-selective agent, during combined sympathetic stimulation and parasympathetic blockade. They also highlight the importance of the vasodilator cholinergic system as a defense mechanism in such situations.

Adrenergic beta-Antagonists↗
PubMed1992

Oral magnesium supplementation improves metabolic variables and muscle strength in alcoholics.

Magnesium deficiency is common among chronic alcoholics, but the knowledge of oral magnesium supplementation to this group is limited. We, therefore, randomized 49 chronic alcoholics, moderate to heavy drinkers for at least 10 years to receive oral magnesium or placebo treatment for 6 weeks according to a double-blind protocol. Effects on metabolic variables and muscle strength were analyzed. Significant reduction of aspartate-aminotransferase (ASAT), alanine-aminotransferase (ALAT) and gamma-glutamyl-transpeptidase (GGT) were seen after magnesium, whereas no change was observed with placebo. Bilirubin decreased in both groups. Serum Na, Ca, and P increased significantly during magnesium therapy compared with no statistically significant change in the placebo group. Serum K and Mg increased slightly after magnesium supplementation and decreased in the placebo group, resulting in a significant difference between the two groups at the end of the study. Muscle strength increased significantly during magnesium treatment, contrasting to no change with placebo. Blood pressure, heart rate, hematological variables, serum lipids (cholesterol, HDL, TG), glucose tolerance, and creatinine were unchanged in the two groups after treatment. Alcohol consumption was similar before and during the trial and does not explain the differences between the two groups The results shows that short-term oral magnesium therapy may improve liver cell function, electrolyte status, and muscle strength in chronic alcoholics.

Administration, Oral↗
PubMed1992

Magnesium deficiency diagnosed by an intravenous loading test.

Magnesium deficiency is common but difficult to diagnose and to assess in clinical practice. The use of a magnesium loading test was therefore evaluated to diagnose magnesium deficiency in 661 hospitalized patients with medical conditions assumed to interfere with magnesium uptake and excretion. Thirty millimoles of magnesium sulphate were administered intravenously during 8 h as a loading test and related to the urinary excretion in the following 24 h. A group of 30 patients without any known predisposition for magnesium deficiency and a group of 27 healthy volunteers served as controls. The mean (with 95% confidence interval) magnesium retention was 4 (-2-10)% in the control group of patients and 3 (-2-8)% in healthy subjects. A significantly higher retention was observed in all the groups of the patients: atrial fibrillation 18 (11-25)%, other arrhythmias 18 (11-24)%, hypertension 27 (20-33)%, coronary artery disease 25 (20-30)%, congestive heart failure 31 (26-37)%, cerebrovascular events 38 (24-51)%, gastrointestinal disorders 22 (14-29)%, diabetes mellitus 16 (9-22)%, and alcoholics 33 (29-36)%. The percentage of patients with a retention greater than mean + 2 SD of the two control groups varied between 22% and 54% among the different patient groups. The mean serum magnesium among the patient groups was similar to the control group of patients, except for the alcoholics, hypertensives and young healthy controls, who had significantly reduced levels. Magnesium retention was significantly correlated to age and renal function, and among the alcoholics negatively correlated to serum magnesium.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

[Cholesterol-lowering effect of oat].

Use of oat-supplement has been advocated to reduce serum cholesterol concentration. In order to study the effect of a daily dietary supplement of oats on lipid levels we performed three controlled clinical trials in healthy Norwegians and patients with hypercholesterolemia. The studies lasted 3-5 weeks, and oats were added to the diet in bread, breakfast cereals, porridge or crispbread. The serum cholesterol concentrations were reduced by 2.5-5% in four of the five groups with an oat-supplemented diet. No effect was found in the group who ate crispbread. Lipid levels remained unchanged in the three control groups. We conclude that oat products have a small but significant cholesterol-lowering effect when given as a supplement to the ordinary Norwegian diet.

Adult↗
PubMed1991

Intrapericardial left atrial aneurysm diagnosed by transoesophageal echocardiography and nuclear magnetic resonance imaging.

A case of intrapericardial left atrial aneurysm is described in a 38-year-old woman, who presented with invalidating paroxysmal atrial fibrillation. The diagnosis was suspected by 2D-echocardiography, and confirmed by transoesophageal echocardiography and magnetic resonance imaging. Chest X-ray, right and left ventricular and coronary angiography were normal. The aneurysm was surgically removed, and the patient has subsequently remained free from symptoms.

Adult↗
PubMed1991

Effects of selective beta 2-adrenoceptor blockade on serum potassium and exercise performance in normal men.

1. The differential effects of beta-adrenoceptor subtypes on potassium fluxes and exercise capacity were compared in eight healthy young men using single oral doses of the selective beta 2-adrenoceptor antagonist ICI-118551, the selective beta 1-adrenoceptor antagonist atenolol or the non-selective beta-adrenoceptor antagonist propranolol. The study was randomized, double-blind and placebo controlled. 2. Potassium in the venous effluent from the exercising muscles increased progressively with increasing exercise intensity. This response was augmented by propranolol, whereas neither atenolol nor ICI-118551 modified the response. After exercise potassium concentration fell exponentially with no difference between the treatment regimens. 3. Cumulative work was significantly reduced by ICI-118551 (6.4%, P = 0.04) and by propranolol (12.4%, P less than 0.01), whereas the reduction with atenolol (5.6%) did not reach statistical significance. 4. Atenolol and propranolol reduced peak heart rate by 23% and 29%, and peak systolic blood pressure by 9% and 11% respectively during maximal exercise. ICI-118551 caused a non-significant reduction in heart rate during submaximal exercise, with a significant reduction at maximum exercise (6% reduction), whereas systolic blood pressure was not different from placebo. Diastolic blood pressures were similar across all treatment regimens. 5. Similar glucose concentrations were obtained at baseline and at exhaustion during all treatment regimens. Lactate concentrations were comparable for any given exercise intensity irrespective of treatment regimens. Propranolol reduced lactate concentrations from the exercising muscles at maximum exercise in proportion to the reduction of maximal exercise capacity. 6. The subjective perception of fatigue was not affected by either beta 1- or beta 2-adrenoceptor blockade.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗
PubMed1989

[Beta blockaders and physical performance. Limiting factors].

Beta blockers are known to cause reduced exercise performance in hypertensive and healthy subjects. Additive effects of selective blockade of beta-1 and beta-2 receptor subtypes seems to account for the total reduction in exercise capacity observed with non-selective beta-1,2 blockade. The mechanism is as yet undefined. The magnitude of the reduction is dependent of type of exercise and level of fitness. Hemodynamic parameters, substrate delivery to the working muscles, mental factors, and interference with potassium homeostasis may be involved.

Adrenergic beta-Antagonists↗
PubMed1989

Effect of beta-adrenergic blockade on hormonal responses during continuous and intermittent exercise.

The modifying effect on exercise performance and neuroendocrine response of the nonselective beta blocker timolol (10 mg b.i.d. for 5 days) and the beta 1-selective beta blocker metoprolol (100 mg b.i.d. for 5 days) was studied. The hormones studied were growth hormone, prolactin, cortisol, renin, epinephrine, dopamine, and norepinephrine. The response was studied during short-term maximal dynamic exercise, using two different exercise protocols; continuous (n = 11) and intermittent (n = 9) bicycle ergometry, in normal healthy young men. Accumulated work on placebo was nearly identical in the two studies, but was significantly reduced by 10.4% and 6.6% with timolol and by 4.7% and 6.7% with metoprolol, during continuous and intermittent exercise, respectively. During continuous exercise, accumulated work was 5.8% lower (p less than 0.05) with timolol than with metoprolol. The hormonal plasma concentrations of all hormones except renin were higher during continuous exercise than during intermittent exercise. Beta blockade had no effect on baseline hormonal levels, but the response was markedly changed during exercise. Maximum epinephrine, cortisol, and prolactin responses increased after beta blockade; dopamine remained nearly unchanged; while the renin responses were attenuated. Norepinephrine concentrations were slightly increased during continuous exercise by beta blockade and rose in direct proportion to the increase in workload. During intermittent exercise, maximum norepinephrine levels were significantly reduced by beta blockade compared with placebo. Thus the effect of beta 1-selective and nonselective beta receptor blockade on circulating hormones does not seem to explain the reduced exercise capacity following beta blockade.

Adrenergic beta-Antagonists↗
PubMed1989

Interaction of naloxone and timolol on maximal exercise capacity and the subjective perception of fatigue.

The effect on exercise performance and on the subjective perception of fatigue of the opioid receptor blocker naloxone, the nonselective beta-blocker timolol, and the combination of these two was studied in a double-blind randomized cycle ergometry test in healthy young men. Cumulative work at exhaustion was reduced by 25% after timolol (P less than 0.002) and by 34% after naloxone/timolol (P less than 0.02) but not after naloxone, compared with placebo. Naloxone alone had no influence on the subjective perception of fatigue (Borg scale rating), but significantly higher ratings were obtained by timolol and by naloxone/timolol. The present study does not support the hypothesis that opioid peptides are of importance for maximal exercise capacity and subjective perception of fatigue during short-term dynamic exercise in healthy young men.

Adult↗
PubMed1989

The importance of potassium and lactate for maximal exercise performance during beta blockade.

Changes in femoral vein pH, lactate, glucose and potassium were studied in a double-blind randomized, short-term, dynamic cycle ergometry exercise test on six healthy male subjects after administration of non-selective (timolol), beta-1-selective (atenolol) beta blocker or placebo. The exercise intensity was increased in steps of 200 kpm/min every 2 min until exhaustion. During submaximal exercise, potassium concentrations in blood from the exercising leg muscles increased progressively with increasing exercise intensity, and was significantly higher for any given exercise level following timolol as compared to placebo administration. The potassium concentrations following atenolol were in-between those of timolol and placebo. Despite reduced working capacity after non-selective beta blockade, almost identical potassium concentrations were reached at exhaustion irrespective of treatment regimens (placebo: 6.3, range 5.8-6.8 mmol/l; atenolol: 6.5, range 6.1-7.3 mmol/l and timolol: 6.4, range 6.2-6.8 mmol/l). The increase in s-lactate concentrations was similar across all treatments, and rose in proportion to the increase in the exercise intensity. A biphasic increase in lactate was observed with identical breaking points (anaerobic threshold) irrespective of treatment regimens. There was no difference in glucose concentrations between the treatment regimens. The marked increase in serum potassium during maximal exercise coincides with leg muscle fatigue and may, by its effect on the muscle cell membrane potential, limit the maximal working capacity following beta blockers. The rise in serum potassium may curtail the use of maximal exercise test as an index of cardiac performance in healthy young subjects.

Adrenergic beta-Antagonists↗
PubMed1988

Difference between beta-1-selective and non-selective beta-blockade during continuous and intermittent exercise.

Limiting factors of maximal exercise performance are not clearly defined. In order to differentiate between various factors, maximal exercise was studied during continuous (n = 12) and intermittent (n = 9) exercise. The non-selective beta-blocker timolol (10 mg b.i.d. for 5 days) was compared double-blind and placebo controlled with the beta-1-selective beta-blocker metoprolol (100 mg b.i.d. for 5 days), with respect to effect on maximal exercise tolerance. Total cumulated work was comparable during continuous and intermittent exercise. Timolol and metoprolol reduced maximal exercise performance. No difference was observed between the two beta-blockers during intermittent exercise. The non-selective beta-blocker caused a greater reduction in exercise performance (10.4%) than the beta-1-selective beta-blocker (4.7%) (P less than 0.05) during continuous exercise. Maximal heart rate was higher with metoprolol than timolol during continuous exercise. The non-selective beta-blocker caused a slightly greater inhibition of lipolysis than the beta-1 selective one. No significant differences in glucose concentrations were observed between the treatment regimens. Exercise caused a marked increase in serum potassium concentrations. Beta-blockade caused further increase in potassium at any given workload. This study indicates that maximal working capacity is comparable during continuous and intermittent exercise. Beta-1-selective and non-selective beta-blockade reduce the maximal working capacity, non-selective more than beta-1-selective. Substrate availability was not responsible for the beta-blocker induced reduction of the working capacity. The rate of rise in serum potassium was significantly higher during beta-blockade and may, therefore, be a limiting factor for the maximal working capacity.

Administration, Oral↗
PubMed1987

The effects of naloxone and timolol on plasma catecholamine levels during short-term dynamic exercise.

In order to study the role of opioid- and betareceptors on exercise-induced catecholamine responses, the effects of acute intravenous administration of 1 and 4 mg naloxone and of the non-selective betablocker timolol 2 mg of on circulating concentrations of adrenalin, noradrenaline and dopamine during exercise to exhaustion were examined in eight normal, healthy young men, using a double-blind, randomized, placebo-controlled design. During maximal exercise, adrenalin levels increased from 71 +/- 17 to 821 +/- 235 pg/ml (p less than 0.05), noradrenaline from 355 +/- 58 to 4235 +/- 1031 pg/ml (p less than 0.05), and dopamine from 72 +/- 20 to 178 +/- 44 pg/ml (p less than 0.05). Naloxone did not influence basal or exercise-induced noradrenaline responses. Timolol clearly augmented peak adrenalin concentration at maximal exercise capacity (1543 +/- 510 pg/ml, p less than 0.05). Basal noradrenaline level was increased (546 +/- 86 pg/ml, p less than 0.05), while exercise-induced noradrenaline level was reduced (2954 +/- 594 pg/ml, p less than 0.05) in proportion to the reduction in maximal exercise capacity during timolol treatment. Neither naloxone nor timolol affected dopamine levels. No additive effect was seen with the combination of naloxone and timolol. It is concluded that the opioid peptides are probably not involved in noradrenaline and dopamine responses, whereas betablockers change the catecholamine response to short-term maximal exercise.

Adrenergic beta-Antagonists↗