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Biomedical subjects

G Olsson

Publications and source records attributed to G Olsson.

At least 73 records · Page 4Linked to original sources
PubMed1991

The supervisory process reflected in dreams of supervisees.

The study supports the notion that what may be concealed in the supervisory process may be revealed in the dreams of supervisees. Supervision as well as patient work mean an intense emotional experience for supervisees, especially for beginners in psychotherapy. This emotional experience was reflected in dreams. The supervisory situation reactivates the supervisees' earlier relationships and problems with authority people. This was also expressed in dreams. Stages in the supervisory process have earlier been described in terms of the learning experiences of the supervisees. The present study provides evidence that the supervisory process should not only be described in terms of different stages of learning, but also in terms of different emotional stages, where especially the beginning and end period mean a strong emotional investment.

Adult↗
PubMed1991

Myocardial infarction. Effects of beta-blockade.

By the mid 1960s a beneficial effect of post-myocardial infarction treatment with beta-blockade had been proposed. However, it was not until 1981 that large clinical trials clearly demonstrated a beneficial effect both in terms of reduction in mortality and morbidity. Today treatment with beta-blockers both in the acute phase of acute myocardial infarction as well as in the stable post-myocardial infarction patient is well established. In this review article, different aspects of early and late treatment with beta-adrenoceptor blockers are discussed. The cardioprotective effects of beta-blockers on mortality and morbidity should not be considered class effects valid for all beta-blockers. Pooled data have clearly demonstrated that beta-blockers with intrinsic sympathomimetic activity have less marked effects. Impressive effects on mortality and morbidity have been obtained with propranolol, timolol, and metoprolol, which are noncardioselective as well as more beta 1-selective (metoprolol), but they are all lacking intrinsic sympathomimetic activity and, furthermore, have a relatively high degree of lipophilicity. It is clear that acute beta-adrenoceptor blockade in suspected acute myocardial infarction reduces mortality and morbidity as well as complications such as chest pain and ventricular arrhythmias during the acute phase. In post-myocardial infarction treatment, it is clear that both mortality and morbidity are reduced. Reports from extended follow-ups after termination of initial double-blind beta-blocker studies in postinfarction patients indicate that withdrawal of the active treatment may increase mortality after cessation of treatment. This is observed despite measures having been taken to avoid so-called acute withdrawal phenomena.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1991

Role of sympathoadrenal medullary activation in the initiation and progression of atherosclerosis.

Clinical and epidemiological investigations provide evidence that psychosocial factors influence the development of coronary heart disease and underlying atherosclerosis, an association that appears to be independent of the effects of other coronary disease risk factors. It has been hypothesized that sympathoadrenal medullary activation mediates behavioral influences on coronary disease, perhaps by potentiation of atherogenesis. This article summarizes four recent studies of the effects of psychosocial stress and sympathetic arousal on atherogenesis in cynomolgus monkeys (Macaca fascicularis) and rabbits. It is reported that socially dominant male monkeys, when fed an atherogenic diet and subjected to periodic social disruption, developed markedly worsened coronary atherosclerosis in comparison with subordinate monkeys; this effect may have been sympathetically mediated, as it was inhibited in similarly aggressive monkeys treated with a beta-adrenergic blocking agent. Studies using chow-fed rabbits demonstrated that exposure to chloralose anesthesia (an agent that provokes profound sympathetic activation) induced endothelial injury (indicated by intracellular accumulation of immunoglobulin G in the aortic endothelium) and abnormal (increased) platelet accumulation. The further observation that these effects were inhibited under beta-adrenoceptor blockade implicates sympathoadrenomedullary arousal in the initiation of atherogenesis. Additionally, sympathetically mediated endothelial damage and increased platelet accumulation occurred preferentially at circumostial sites in the rabbits, a finding consistent with the hypothesis that the hemodynamic concomitants of sympathetic activation contribute to atherogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Medulla↗
PubMed1991

Prevention of sudden death using beta-blockers. Review of possible contributory actions.

Coronary artery disease is the most serious complication of hypertension; therefore, the treatment of hypertension should be directed toward reducing the mortality from this disease. Since the majority of deaths occurring in post-myocardial infarction patients and hypertensive patients are sudden, the key objective is coronary artery disease treatment that will reduce the risk of sudden death. Several pharmacological interventions have been tested to determine whether they reduce the risk of sudden death. So far, only treatment with beta-adrenoceptor antagonists has been proven effective. Since most sudden cardiac deaths are due to ventricular fibrillation, an antifibrillatory effect on beta-adrenoceptor blockade has been invoked and demonstrated in clinical as well as animal experimental studies. Apart from an antifibrillatory effect, other effects of beta-blockade may also be involved. In the present review, different effects of beta-blockers that may contribute to the observed beneficial effects are discussed. The reduction in the risk of sudden death during active beta-adrenoceptor blockade reported in clinical studies is probably related to the summation of different effects, since cardiovascular drugs with a more limited mode of action (i.e., pure anti-ischemic effect or pure antiarrhythmic effect) have not shown similar impressive results.

Adrenergic beta-Antagonists↗
PubMed1991

Fibrinogen and plasminogen activator inhibitor-1 levels in hypertension and coronary heart disease. Potential effects of beta-blockade.

The roles of fibrinolysis, fibrinogen, and plasminogen activator inhibitor-1 in the development of coronary heart disease are reviewed, and possible effects of long-term treatment with beta-blockade are discussed. Decreased fibrinolysis is associated with coronary artery disease, and coronary thrombus formation is the most frequent event precipitating myocardial infarction. Recently, it has also been shown that high levels of fibrinogen and plasminogen activator inhibitor-1 are predictors for myocardial infarction. Because beta-blockers are used to treat hypertension, angina, and myocardial infarction, it is important to determine the impact of beta-blockers on fibrinolysis. Several factors influence fibrinolysis. Some forms of stress and epinephrine infusions increase fibrinolysis, probably by stimulating beta 2-adrenoceptors. Nonselective beta-blockers may adversely affect this process, whereas beta 1-selective antagonists and those with intrinsic sympathomimetic activity may not. Since prostacyclin synthesis is correlated to increased fibrinolytic activity and since beta-blockers may moderate stress-induced reductions in prostacyclin formation, beta-blockers may have the potential to exert a beneficial effect on fibrinolysis in chronic stress situations. The net effect of beta-blockade is not easily predicted and probably depends on the nature of the stress (whether it is acute or chronic), the status of the patient, and the selectivity of the beta-blocker. Nevertheless, it remains a possibility that beta-blockers may exert a positive therapeutic effect in relation to coronary thrombosis by an action on fibrinolytic mechanisms.

Adrenergic beta-Antagonists↗
PubMed1991

Is there an optimal prophylactic nitrate therapy?

Nitrates have a place in the prophylactic treatment of patients with angina pectoris. Their efficacy is not in doubt. However, there may be some practical problems associated with their use, such as unreliable absorption, short duration of action, treatment-induced headache, development of nitrate tolerance and a suggested rebound phenomenon observed during intermittent dosing. This article discusses how many of these problems may be solved by selection of formulation as well as nitrate compound. Thus, the development of a controlled-release formulation producing sufficiently high nitrate plasma concentrations during part of the day, followed by a low nitrate level rather than a nitrate-free interval, seems to have the potential to prevent both nitrate tolerance and rebound phenomenon. This system would also offer a sufficiently long duration of action with a convenient once-daily dose regimen.

Angina Pectoris↗
PubMed1990

Influence of metoprolol treatment on sympatho-adrenal activation of fibrinolysis.

The effects of mental stress (a colour word conflict test, CWT) and adrenaline infusions (0.1 and 0.4 nmol kg-1 min-1) on t-PA activity, t-PA antigen, PAI-1 activity and PAI-1 antigen were studied in 18 healthy male volunteers. Furthermore, the effects of metoprolol (200 mg/day during 1 week) or placebo (double-blind cross-over study) on fibrinolytic responses to sympatho-adrenal activation, and relationships between fibrinolysis and blood lipids were investigated. Low and high dose adrenaline infusions yielding plasma adrenaline levels of 0.9 +/- 0.1 and 3.4 +/- 0.4 nmol/l, respectively, dose-dependently increased t-PA levels with a concomitant decrease in PAI-1 levels. A similar, but weaker, fibrinolytic response seemed to occur during CWT, when plasma adrenaline levels were only moderately increased (to 0.4 +/- 0.1 nmol/l). Metoprolol treatment did not influence the resting levels of the fibrinolytic variables studied, but tended to enhance the t-PA response to CWT and further reduce PAI-1 during adrenaline infusion. Metoprolol treatment was not accompanied by any rise in PAI-1 levels despite drug induced elevations of triglyceride levels. Thus, the present study shows that sympatho-adrenal activation increases fibrinolytic activity in vivo and that metoprolol treatment may have a favourable influence on this activity.

Adrenal Glands↗
PubMed1990

A double-blind comparison of metoprolol CR/ZOK 50 mg and atenolol 50 mg once daily for uncomplicated hypertension.

In a double-blind study with parallel groups, the clinical bioequivalence of the antihypertensive effect of metoprolol CR/ZOK (controlled release formulation) 50 mg and atenolol 50 mg in ordinary tablets given once daily for uncomplicated hypertension was investigated. Clinical bioequivalence was defined as difference in blood pressure reduction less than 8 mmHg. The study involved 195 patients, 98 on metoprolol CR/ZOK and 97 on atenolol. All patients were taken off antihypertensive therapy during a 2-week placebo run-in period. Thereafter the patients were randomly allocated to metoprolol CR/ZOK 50 mg or atenolol 50 mg for 4 weeks. In patients with a diastolic blood pressure remaining above 90 mmHg, the dose was increased to 100 mg daily of the respective drug. After 4 weeks treatment with 50 mg of the two therapies, blood pressure and heart rate was significantly reduced in both treatment groups. At this dose, clinical bioequivalence was found regarding both blood pressure and heart rate reductions. After 8 weeks of therapy (100 mg doses given to 31 in the metoprolol group and 43 in the atenolol group), clinical bioequivalence according to stated definition was found for blood pressures and heart rate reductions, although the reductions of systolic and diastolic blood pressures at rest as well as diastolic blood pressure during exercise were significantly greater in the metoprolol group. In an evaluation of the responder rate after the 8 weeks of treatment, 89% of the patients in the metoprolol CR/ZOK group and 74% in the atenolol group (P less than .05) had a diastolic blood pressure reduction to 90 mmHg or less.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Long-term cardiovascular effects of metoprolol therapy: a review article.

Long-term studies in primary and secondary prevention using metoprolol have showed improvement in prognosis. This review summarizes the clinical results of such studies, and puts these results into the perspective of findings in mechanistic and explanatory studies. Many possible factors may have contributed to explain the beneficial effects on prognosis. The antihypertensive action, cardiac anti-ischemic action, antifibrillatory action, antiatherogenic and antithrombotic actions of metoprolol are discussed. The additive effects of these actions may explain the clinically observed beneficial effects. In the evaluation of a specific intervention, it is important to realize the multiple actions that may contribute, and not only discuss single factors.

Animals↗
PubMed1990

Influence of metoprolol CR/ZOK on plasminogen activator inhibitor (PAI-1) in man: a pilot study.

Recent primary and secondary preventive trials have shown that long-term metoprolol therapy reduces the risk of acute cardiovascular complications. To test whether part of this beneficial long-term effect may be due to effects on the fibrinolytic system, three pilot studies were performed; two in healthy individuals, and one in patients with mild hypertension or uncomplicated atrial fibrillation. The effect of metoprolol CR/ZOK (controlled release) 100-200 mg daily, on plasminogen activator inhibitor activity (PAI-1) in plasma was measured. In addition serum triglycerides and orosomucoid were analyzed. All the individuals were included in double-blind placebo controlled cross-over trials with treatment periods ranging from 4 days to 3 weeks. During metoprolol therapy PAI-1 values were reduced, while orosomucoid and triglyceride levels were unchanged. A linear inverse correlation was found between fibrinolysis and PAI-1 activity in plasma, indicating that PAI-1 activity serves as an indicator of fibrinolysis. PAI-1 activity and triglycerides were significantly correlated during placebo and metoprolol therapy. In conclusion, our results in these pilot studies suggest that metoprolol enhances fibrinolytic activity as seen by reduced PAI-1 activity. These results should be further confirmed and put into relation of clinical effects of the therapy.

Adult↗
PubMed1990

Platelet aggregability in humans: contrasting in vivo and in vitro findings during sympatho-adrenal activation and relationship to serum lipids.

Platelet aggregability was studied in 18 healthy volunteers during mental stress (a colour word test; CWT) and low- and high-dose adrenaline infusions using an ex vivo technique (filtragometry) and conventional in vitro aggregometry. CWT and high-dose adrenaline (3.4 nmol l-1 in plasma) shortened filtragometry readings, suggesting increased platelet aggregability in vivo. Low-dose adrenaline had no effect despite higher adrenaline levels in plasma (0.9 nmol l-1) than during CWT (0.4 nmol l-1). Platelet sensitivity to ADP in vitro was reduced following CWT and further reduced following adrenaline infusions. In vitro, adrenaline (50 nmol l-1) had little effect on platelet aggregation per se, but enhanced aggregability evoked by ADP (at ED50). Adrenaline potentiation of ADP-induced aggregation was enhanced after CWT, but was not related to filtragometry responsiveness to stress in vivo. Serum LDL-cholesterol levels were inversely correlated to filtragometry readings at rest, suggesting an adverse influence on platelet aggregability in vivo. HDL-cholesterol levels were inversely correlated to platelet sensitivity to ADP in vitro, suggesting a positive influence. Thus, sympatho-adrenal activation enhances platelet aggregability in vivo (as assessed by ex vivo filtragometry), but adrenaline alone cannot explain the pro-aggregatory effect of mental stress. Serum lipoprotein alterations associated with increased risk for atherosclerosis seem to enhance platelet aggregability. The conventional in vitro technique may poorly reflect platelet aggregability in vivo.

Adult↗
PubMed1990

Effects of prolonged adrenaline infusion and of mental stress on plasma minerals and parathyroid hormone.

The role of the sympatho-adrenal system for the secretion of PTH in humans is not established. Previous studies on the effects of adrenaline on plasma mineral homeostasis have focused on injections or short-term infusions of adrenaline, and conflicting results concerning calcium and parathyroid hormone (PTH) responses have been reported. We therefore infused adrenaline or placebo continuously for 3 h to 10 healthy volunteers and studied several plasma minerals, as well as PTH levels. Venous plasma adrenaline concentrations increased to the upper physiological range (5 nmol l-1) during adrenaline infusion. Another nine volunteers were exposed for 25 min to mental stress (a colour word conflict test; CWT), which causes marked circulatory changes and raises plasma catecholamine concentrations. Plasma ionized and total calcium, and magnesium concentrations were slowly and gradually reduced during infusion of adrenaline, but there was only a small increase in PTH. Plasma potassium was decreased by adrenaline within 30 min and thereafter did not change further during infusion. There was a marked but transient increase in the plasma free fatty acids concentration, which were not related to the reduction of the calcium or magnesium levels. The adrenaline-induced decrements in calcium, magnesium and potassium, and increases in heart rates persisted 30 min after the infusion, despite a rapid decrease in plasma adrenaline concentrations within 5 min of termination of the infusion. Plasma phosphate concentrations were lowered during the first 90 min of adrenaline infusion, but after 3 h they had returned to baseline despite continued infusion. CWT induced small increments of the plasma ionized calcium and PTH concentrations. Plasma potassium levels were raised despite increases in plasma adrenaline at the beginning of the stress test, while phosphate values were reduced at the end of the test. Thus, long-lasting elevations of circulating adrenaline lower plasma ionized and total calcium, phosphate, magnesium and potassium, but the time courses for these changes differed markedly. Despite the reduction of plasma ionized calcium there was only little increase in PTH and thus no indication that sustained elevations of circulating adrenaline stimulates the secretion of PTH in vivo in humans. Responses to acute mental stress and adrenaline infusion differed qualitatively, indicating that adrenaline responses to stress are of minor importance in this respect.

Adult↗
PubMed1990

Pyrite oxidation by thermophilic archaebacteria.

Three species of thermophilic archaebacteria of the genera Sulfolobus (Sulfolobus acidocaldarius and S. solfataricus) and Acidianus (Acidianus brierleyi) were tested for their ability to oxidize pyrite and to grow autotrophically on pyrite, to explore their potential for use in coal desulfurization. Only A. brierleyi was able to oxidize and grow autotrophically on pyrite. Jarosite was formed during the pyrite oxidation, resulting in the precipitation of sulfate and iron. The medium composition affected the extent of jarosite formation.

Archaea↗
PubMed1990

Coronary artery disease can be prevented by antihypertensive therapy: experiences from the MAPHY Study.

The present randomized primary prevention study in hypertensive men aged 40-64 years (n = 3,234) was aimed at investigating whether metoprolol given as initial treatment would prevent coronary artery disease (CAD) better than thiazide diuretics. Two hundred fifty-five patients had a definite CAD event during the 15,730 patient-years of follow-up; 25% of these events were fatal, and 38% were definite acute myocardial infarctions. The incidence of CAD was significantly lower during follow-up in patients randomized to metoprolol than in patients randomized to diuretics: 111 vs. 144 cases (p = 0.001). Stroke mortality was significantly lower in the metoprolol group than in the diuretic group, but the overall stroke incidence was similar in the two treatment groups. A majority of events occurred among smokers in both treatment groups although only one-third of patients were smokers at baseline. Blood pressure (BP) control was similar in the two treatment groups; therefore, the difference between the groups in CAD events is mediated via mechanisms other than the BP-reducing effect of metoprolol.

Adult↗
PubMed1989

Treatment of ventricular arrhythmias in the coronary patient: what sort of patient? For which rhythm disorder? With which procedure?

In the patient with coronary artery disease, complex ventricular arrhythmias and frequent ventricular arrhythmias appear to be independent risk factors for subsequent death, particularly in patients who have had myocardial infarction. In patients with symptomatic arrhythmias, treatment must be instituted and tested during rigorous supervision of the patient. Using both the noninvasive Holter monitoring/exercise test procedure and invasive electrophysiologic testing, a beneficial antiarrhythmic response after institution of antiarrhythmic agents indicates improved prognosis. However, a negative treatment response during programmed stimulation does not necessarily indicate bad prognosis. This is particularly true for testing during amiodarone treatment. For unselected patients, routine antiarrhythmic treatment cannot currently be recommended. Continuing studies will show whether screening for electrical instability of the myocardium, and institution of antiarrhythmic therapy thereafter, will improve overall survival. If patients tolerate beta-blocking treatment, this should probably be instituted because reductions in mortality have been found, particularly in high-risk patients.

Anti-Arrhythmia Agents↗
PubMed1989

[Injury patterns in Danish competitive swimming].

A total of 432 Danish competitive swimmers were asked to complete a questionnaire about the epidemiology of injuries sustained during swimming in the season of 1986/1987. Two hundred and sixty-eight (62%) replied. We found a total of 100 injuries in 80 swimmers with an incidence of 0.9 injuries per swimmer per 1,000 hours of swimming, and a point prevalence of 15% on the day of competition. The shoulder, the back and the knee joint were most commonly involved. No particular swimmingstroke was associated with a greater risk of injury. There was, however, a tendency for butterfly swimmers to have more frequent shoulder injuries and for breaststroke swimmers to have more frequent knee-injuries. Medal winners were significantly more frequently injured. Half of the injured swimmers were seen by a doctor.

Adolescent↗