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At least 1,639 records · Page 91Linked to original sources
PubMed1989

[Long-term treatment of hypertension with a selective beta-1-blockader without sympathomimetic activity. II. Changes in the structure and function of the left ventricle].

The effect of the 6 months long treatment with the Hungarian selective beta-1-blocker Betaloc (Metoprolol) on the structure and function of the left ventricle was studied in 30 hypertensive patients--II stage (with echocardiographically proved left ventricular hypertrophy) by means of simultaneous recording of M-type echocardiogram, ACG, PCG and ECG. The telediastolic thickness of the septum and the posterior wall and the left ventricular muscular mass decrease at the end of the 6-th month (p less than 0.0001). The telesystolic dimension and volume decrease (p less than 0.0001) in the 6-th month without changes in the telediastolic dimension and volume (p greater than 0.32). The shortening fraction and the ejection fraction increase (p less than 0.0001), Vcf increases insignificantly (p greater than 0.05). The isovolumetric relaxation shortens (p less than 0.0001), the active suction period lengthens (p less than 0.0001) as well as the fast filling period (p less than 0.0027). By controlling the arterial pressure and suppressing the sympathetic stimulation of the heart the prolonged Betaloc treatment leads to reversion of the hypertrophy and improves the left ventricular function.

Cardiomegaly↗
PubMed1989

[Clinical significance of intrinsic sympathomimetic activity of the beta blocker carteolol. II: Comparative studies of carteolol and pindolol in patients with bradycardia].

Completing previous studies in patients with sinus bradycardia (Med. Klin. 82 [1987], 647-650) we compared metoprolol with carteolol and pindolol, pindolol with carteolol, no treatment with carteolol (in two groups) in five series of the paired comparisons of Holter-ECG each. With change from metoprolol to carteolol or pindolol (dose ratio 10:1) lowest heart rate on Holter-ECG increased by 28 or 29% without change of exercise heart rate. Direct comparison of pindolol and carteolol revealed a very similar heart rate profile, indicating equipotent beta blockade and ISA. In patients with previous beta blocker induced bradycardia, carteolol did not change a normal resting heart rate off treatment. However, in patients with spontaneous sinus bradycardia carteolol increased lowest heart rate (+14%, due to overriding ISA) and lowered exercise heart rate (-15%, due to overriding beta blockade). A beta blocker induced sinus bradycardia consistently improved with change of treatment to carteolol and pindolol. With caution carteolol and pindolol may also be used despite spontaneous sinus bradycardia.

Adult↗
PubMed1978

[Pharmacological study of para-aminoclonidine, an alpha sympathomimetic].

Para-aminoclonidine is a more potent alpha-adrenergic agent than clonidine; in vitro on Rat aorta it is 150 times more active than NE, in vivo on pithed Rat it is still twice as active. The hypotensive action of paraaminoclondine is only manifested when given intraventricularly. In the conscious Rat, it has a diuretic action when given per os. Following IV injection in the anaesthetized Dog, the para-aminoclonidine induces an essentially hydric diuresis which is independet of its hypertensive action.

Adrenergic alpha-Agonists↗
PubMedDate not supplied

[Effect of corticosteroids on the action of sympathomimetics].

Corticosteroids restore the bronchial responsiveness to beta-adrenergic stimulants in man. This has been shown both in severe asthmatic patients and in normal subjects, rendered insensitive by artificial means. On the contrary, in patients with bronchial asthma who have airways reactive to beta-adrenergic stimulants, the combination of corticosteroids and sympathicomimetics results in an additive effect of their bronchodilating capacity. Animal models, both in vivo and in vitro, show the same type of interaction between corticosteroids and beta-adrenergic stimulants. The mechanism by which corticosteroids restore the bronchial sensitivity to beta-adrenergic stimulation is not completely understood. Several mechanisms may be involved such as increased agonist binding, decreased receptor turn-over, increased uncoupling between receptor and adenylcyclase, decreased extraneuronal uptake, decreased COMT-activity. The relevance of the influence of corticosteroids on the metabolism of membrane phospholipids remains highly speculative.

Adrenal Cortex Hormones↗
PubMedDate not supplied

[Effect of prolonged beta-adrenergic treatment on the ventilatory response to sympathomimetics].

Ventilatory adrenergic responsiveness induced by long-term beta-mimetic treatment over three years were analysed in a study carried out in two groups of asthmatics. In group I, 11 patients received theophylline and oral beta-2-agonists; in group II, 7 patients received the same drugs and corticosteroids. Pulmonary function tests were serially performed with a body plethysmograph (Jaeger). The effect of beta adrenergic stimulation with 400 micrograms fenoterol was measured using variations of flow-volume curves. The mean increase of FEV1 after fenoterol was: in group I, 0.680 +/- 0.200 1 before treatment and 0.500 +/- 0.340 1 after beta adrenergic therapy; in group II, it was 0.550 +/- 0.340 1 before treatment and 0.510 +/- 0.350 1 after treatment (difference not statistically significant). For each patient, FEV1 variations were expressed in percent of optimum improvement. In most cases, there was a significant correlation between the two parameters (0.38 less than r less than 0.59), but the slopes of the regression curves differed from one patient to another. Intra-individual variation coefficient of the improvement of FEV1 has been calculated and showed large variations of the adrenergic pulmonary responses: from 34% to 98% of the mean improvement. Four patients only exhibited a significant and definitive decrease of their adrenergic response, which could be due to tachyphylaxis. But a transient loss of responsiveness to adrenergic stimulation has been found in all patients. Those cases were related to viral infections or allergen inhalations.

Adrenal Cortex Hormones↗
PubMed1988

Comparison of thermogenic activity induced by the new sympathomimetic Ro 16-8714 between normal and obese subjects.

In a previous study, we demonstrated that the new beta-adrenoceptor agonist Ro 16-8714 possesses thermogenic property in normal male volunteers. The aim of the present study was to compare the metabolic response of lean vs obese individuals to a similar dose of this compound. Following an overnight fast, Ro 16-8714 (0.17 mg/kg fat free mass) or a placebo was given per os to six normal-weight subjects and to six moderately obese subjects. The rate of energy expenditure (EE) and the substrate utilization were determined by indirect calorimetry (hood system) before and for 6 h following the drug administration. Heart rate and blood pressure as well as plasma glucose, insulin and free fatty acid (FFA) concentrations were also measured at regular intervals throughout the study. The increment relative to base-line (mean +/- s.e.m.) in EE was similar in the two groups and averaged 4.0 +/- 1.4 per cent and 12.2 +/- 1.4 per cent with placebo and with Ro 16-8714 respectively in lean subjects, whereas the values reached 3.5 +/- 1.2 per cent and 14.4 +/- 2.0 per cent in obese subjects. Heart rate, systolic blood pressure, insulin and FFA were increased without any significant difference between the two groups. This study shows that Ro 16-8714 is a potent thermogenic agent both in normal and obese subjects.

2-Hydroxyphenethylamine↗