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Biomedical subjects

K Eliasson

Publications and source records attributed to K Eliasson.

At least 37 records · Page 2Linked to original sources
PubMed1986

Personal control over work pace--circulatory, neuroendocrine and subjective responses in borderline hypertension.

Cardiovascular and neuroendocrine reactivity during arithmetic task performance were studied in 24 patients with borderline hypertension and normotensive controls. Personal control (self-paced versus externally paced performance) resulted in an attenuated blood pressure (BP) response to task performance in normotensives but not in borderline hypertensives. In response to self-paced work, systolic blood blood pressure (SBP) reactivity was significantly greater in borderline hypertensives, but the heart rate (HR) reactivity was similar in borderline hypertensives and normotensives under the different pacing conditions. Task difficulty (pace variation during external pacing) did not differentially affect reactivity in borderline hypertensives and normotensives. Venous plasma noradrenaline and adrenaline were unaffected by task performance. At rest after the task performance plasma noradrenaline was elevated in both normotensives and borderline hypertensives. The latter group also showed a persistent elevation of diastolic blood pressure after task performance, suggesting a prolonged vasoconstrictor response. The present findings indicate that, in terms of circulatory responses, borderline hypertensives may profit less than normotensives from personal control over environmental demands.

Adult↗
PubMed1986

Reactivity to mental stress and cold provocation during long-term treatment with metoprolol, propranolol or hydrochlorothiazide.

In a study aimed at comparing the effects of beta-blockers and thiazide diuretics on responses to stressful provocations, 45 essential hypertensives (WHO I-II) were treated with either the selective beta-blocker metoprolol (METO), the non-selective beta-blocker propranolol (PROP) or hydrochlorothiazide (HTZ) for 6 months. Blood pressure, heart rate and plasma catecholamines were measured in connection with a mental stress test and a cold pressor test before and during therapy. All drugs reduced outpatient blood pressure similarly, but beta-blockade reduced blood pressure and heart rate levels more efficiently at rest and during stress in the laboratory. Heart rate reactivity to stress was reduced mostly by beta-blockade during mental stress. Blood pressure and sympatho-adrenal reactivity were unchanged by therapy. Stress reactivity failed to predict antihypertensive responses. The results suggest that beta-blockade may be more effective than diuretic treatment in reducing blood pressure levels and cardiac workload as assessed by the rate pressure product in stressful situations.

Adult↗
PubMed1985

Effect of beta 1-selective and nonselective beta blockade on blood pressure relative to physical performance in men with systemic hypertension.

Eleven physically active men with systemic hypertension were studied after 5 weeks of treatment with placebo, atenolol or propranolol. A double-blind, crossover randomized design was used. Blood pressure (BP), heart rate (HR), physical performance capacity, rate of perceived exertion and blood lactate concentrations were measured during rest, exercise to exhaustion and postexercise, at 8 and 24 hours after intake of the last dose. Blood pressure at rest and during exercise was similarly decreased with both drugs (8 and 24 hours), and there was no difference between 8 and 24 hours with any of the treatments. Heart rate (8 hours) was decreased similarly by both drugs, but after 24 hours, HR at increased workloads (above 120 watts) was higher with atenolol compared with propranolol. Maximal HR was lower with propranolol than atenolol at both 8 and 24 hours. Maximal exercise loads (8 and 24 hours) were 231 and 232 watts with placebo, 211 and 212 with propranolol and 228 and 227 with atenolol. That is, maximal workload was decreased with propranolol compared with placebo and atenolol at both 8 and 24 hours. No difference was found between placebo and atenolol at either 8 or 24 hours. The rate of perceived exertion values were higher with propranolol than atenolol. Blood lactate concentrations did not differ according to treatments. The results indicate that atenolol, when given in a dose that decreases resting and exercise BP to the same extent as propranolol, limits physical performance less than propranolol.

Adult↗
PubMed1985

Effects of long-term therapy with labetalol on lipoprotein metabolism in patients with mild hypertension.

The effects of labetalol on serum lipoproteins, the intravenous fat tolerance test (IVFTT) and lipoprotein lipase (LPL) and hepatic lipase (HL) activities were studied in 16 patients with mild hypertension before and after 6 months of therapy. Most patients were found to be normotensive on 200 mg labetalol/day. Before therapy the mean concentration of serum TG was 0.75 +/- 0.21 (SD) mmol/l, of total cholesterol 5.41 +/- 1.25 mmol/l and of HDL cholesterol 1.67 +/- 0.61 mmol/l. After labetalol no significant changes were found in the concentrations of TG and cholesterol in the VLDL, LDL and HDL fractions. The mean values for the IVFTT and for LPL and HL activities were in the normal range and remained unchanged during therapy.

Adult↗
PubMed1985

Borderline hypertension. Circulatory, sympatho-adrenal and psychological reactions to stress.

The purpose of this study was to examine circulatory and sympatho-adrenal responsiveness in borderline hypertensives compared to established hypertensives and normotensive controls under conditions of physical and mental provocation. Measurements of plasma catecholamines or the urinary excretion of their metabolites were used as indicators of sympathetic activity and psychological variables were assessed by means of self-ratings. There were several signs of an increased neurogenic influence in borderline hypertensives. Urinary catecholamine excretion was related to body measures only in this group. During mental stress, induced by a filmed version of Stroop's colour word test, there were signs of an enhanced hypothalamic defence reaction in the borderline group, as judged by increased circulatory responses and higher plasma adrenaline levels. These signs of increased arousal could be associated with a tendency to compensate for a slightly decreased accuracy in task performance compared to controls by increasing effort. This led to a negative relationship between subjective stress and performance, present only in the borderline group. In another group of borderline hypertensives, the effects of personal control over work pace were compared to normotensives. Personal control reduced circulatory responses to mental arithmetics in controls, but had no beneficial effect in the borderline group. Also in this study, there were signs of an enhanced defence reaction in borderline hypertensives. Higher arousal levels in borderline hypertensives may, theoretically, be explained by personality differences. During an isometric handgrip test, borderline hypertensives showed a tendency towards increased alpha-adrenergic vasoconstriction compared to both established hypertensives and controls. A somewhat higher diastolic blood pressure variability, lower plasma volume and higher venous tone compared to normal also suggest increased neurogenic influences in borderline hypertension. There are similarities between the borderline hypertensive state and the circulatory and sympatho-adrenal pattern of the hypothalamic defence reaction. An enhancement of this reaction is particularly evident during mental stress, whereas somatic provocations such as an orthostatic test, a cold pressor test and physical work produce more similar responses compared to established hypertensives and controls. An increased reactivity to mental stress, especially when personal initiative is challenged, may contribute to the increased cardio-vascular morbidity of borderline hypertensives as a group.

Adrenal Glands↗
PubMed1984

Therapeutic and metabolic effects of sotalol.

In a single-blind, randomized study, the cardiovascular and metabolic effects of sotalol, 40 to 160 mg/day, in six patients with mild essential hypertension were compared to those of placebo at rest and during submaximal dynamic exercise. Resting blood pressure was controlled by sotalol but not the pressor response to exercise, despite reduction of tachycardia. The major metabolic finding on sotalol was an approximately 40% decrease in lipid mobilization during exercise. Alterations in muscle lactate concentrations were much like those caused by other beta-blockers. Plasma concentrations of norepinephrine and epinephrine were doubled during exercise on sotalol, epinephrine disposition more so. No effects on serum lipoproteins were observed after 6 wk on sotalol in therapeutic doses. Despite its special electrophysiologic properties, sotalol appears to induce the same cardiovascular and metabolic changes during exercise as do other beta-blockers.

Adult↗
PubMed1984

Urinary catecholamine metabolites in borderline and established hypertension. Relationship to body composition.

The urinary excretion of catecholamine metabolites was studied by means of gas chromatography-mass spectrometry in 38 hypertensive patients on a moderately sodium-restricted diet during hospitalization. Twenty-four patients had established hypertension (EHT) and 14 borderline hypertension (BHT) with mean basal morning blood pressures of 155 +/- 14/101 +/- 8 and 132 +/- 9/87 +/- 4 mmHg, respectively. In these two groups of hypertensive patients the mean daily excretion of 4-hydroxy-3-methoxymandelic acid (VMA) was 13.3 +/- 5.9 vs. 14.0 +/- 6.3 nmol/ml and of 4-hydroxy-3-methoxy-phenylglycol (HMPG) 7.8 +/- 4.1 vs. 7.0 +/- 3.9 nmol/ml. These concentrations were not significantly different from the corresponding values of 18 normotensive control persons (mean ambulatory blood pressure 121 +/- 10/74 +/- 9 mmHg, VMA 12.3 +/- 5.5 nmol/ml, HMPG 9.6 +/- 3.9 nmol/ml). The normotensive individuals excreted 23.7 +/- 8.9 nmol/ml of homovanillic acid (HVA), while the two groups of hypertensive patients showed significantly lower HVA excretion, EHT 17.6 +/- 6.2 nmol/ml and BHT 16.1 +/- 5.9 nmol/ml (p less than 0.05). Our findings support the view that no generalized increase in sympathetic activity exists in EHT or BHT. In BHT, but not in EHT, there were correlations between catecholamine metabolite excretion and body weight. The biological significance of the lower HVA concentrations in hypertensive patients compared to control individuals is not clear.

Adult↗
PubMed1984

Raynaud's phenomenon caused by beta-receptor blocking drugs. Improvement after treatment with a combined alpha- and beta-blocker.

Twenty-four hypertensive patients reported vasospastic symptoms in their hands during treatment with beta-blocking drugs with different pharmacological properties. Twenty patients had symptoms when staying indoors and 11 did not always experience complete relief of symptoms following active rewarming attempts. Finger systolic blood pressures were measured after standardized local cooling. In 15 patients, blood pressure decreased to a pathological level during this procedure. Previous beta-blockade was changed to combined alpha- and beta-blockade with labetalol given twice daily in a mean dose of 259 mg/day for 3 months. After this period, most patients showed a decreased temperature sensitivity both objectively and subjectively. Blood pressure control was maintained at the previous level. Heart rate increased significantly during treatment with labetalol. Labetalol offers an alternative treatment to patients suffering from vasospastic side-effects of beta-blockers.

Adrenergic beta-Antagonists↗
PubMed1983

Circulatory and sympatho-adrenal responses to stress in borderline and established hypertension.

Responses to mental stress [a colour word test (CWT), orthostatic testing (ORT) and a cold pressor test (CPT) were studied in 33 subjects with essential hypertension (EHT), 16 subjects with borderline hypertension (BHT) and 17 age and sex-matched normotensive controls (NT). Venous plasma noradrenaline (NA) was similar in all groups. CWT induced marked circulatory responses and metabolic activation with minor increases in NA. Circulatory and NA responses to ORT and CPT were similar in all groups. CWT elevated diastolic blood pressure more in BHT and tended to elevate HR more in EHT and BHT than in NT. Plasma adrenaline (ADR) tended to be higher in BHT and increased during all provocations in EHT and BHT but not in NT. Early hypertension appears to be associated with enhanced cardiovascular and sympatho-adrenal reactivity (resembling a hypothalamic defence reaction) which is revealed by mental stress, rather than stimuli such as ORT or CPT. Venous plasma NA has limitations in defining neurogenic alterations in hypertension since it reflects poorly sympathetic activity in the organs responsible for pressor responses to emotional stimuli. Plasma ADR is more valuable in this respect.

Adolescent↗
PubMed1983

Efficacy and tolerability of hydralazine, in conventional and slow-release preparations, during long-term treatment of primary hypertension.

In 23 patients with primary hypertension, the efficacy and tolerability of slow-release hydralazine administered once daily were compared with those of conventional hydralazine given two to four times a day. All patients were treated concomitantly with beta-blockers, diuretics, or both. Blood pressure control achieved with multiple doses of conventional hydralazine was maintained with slow-release hydralazine, with no discrepancy between once- and twice-daily administration, when the same daily dose of hydralazine was given. A differentiated method of assessing tolerability demonstrated no differences between the hydralazine formulations and dose regimens in the incidence of side effects. This finding indicates that larger single doses than are normally given with hydralazine can be given with slow-release hydralazine without increased risk of side effects.

Adult↗
PubMed1982

Peripheral vasospasm during beta-receptor blockade - a comparison between metoprolol and pindolol.

Ten men reported vasospastic symptoms in their hands during metoprolol treatment. They had no signs of occlusive arterial disease. The temperature reaction to local cooling was measured and no improvement was found after changing to pindolol. Vasospastic symptoms during beta-receptor blockade may arise in predisposed individuals irrespective of the type of beta-receptor antagonist used.

Adult↗
PubMed1981

Serum lipoprotein changes during atenolol treatment of essential hypertension.

Serum lipoproteins were determined in 15 patients before and during antihypertensive treatment with atenolol (0.1-0.2 g/day for a mean of 8 months. The mean blood pressure fell from 171/103 to 154/93 mm Hg (p less than 0.05). Significant lipoprotein changes were an increase in very low density triglycerides (VLDL-TG) from 1.21 +/- 0.95 (SD) to 1.62 +/- 1.24 mmol/l (p less than 0.01) and in low density (LDL) TG from 0.46 +/- 0.12 to 0.51 +/- 0.12 mmol/l (p less than 0.05). Together, these TG increases resulted in development of hypertriglyceridaemia in 7/15 patients during atenolol treatment. No effect on whole serum cholesterol or on the high density lipoprotein cholesterol concentrations were found. Thus, some patients on long term treatment with atenolol seem to received the benefit of normotension at the cost of hypertriglyceridaemia. This may have practical implications, since hypertriglyceridaemia, constitutes an important risk factor for atherosclerosis.

Atenolol↗
PubMed1981

Erythrocyte and total body potassium in untreated primary hypertension.

In a study of total body and erythrocyte potassium in mild hypertension we found decreased intracellular potassium concentrations in 41 hypertensives compared to controls but no correlation between intracellular potassium, measured by whole body counting, and erythrocyte potassium. A total body potassium corresponding to an intracellular potassium of 85% or less of the expected value was found in females. In the hypertensives, a negative correlation existed between serum and erythrocyte potassium. No correlation was found between potassium decrease and urinary aldosterone or plasma renin level. An inhibition of the active sodium-potassium exchange at the cellular level is proposed as an explanation of these findings.

Adult↗