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At least 181 records · Page 10Linked to original sources
PubMed1985

Short-term effects of beta-adrenoceptor blocking drugs with and without cardioselectivity and intrinsic sympathomimetic activity on lipoprotein metabolism in hypertriglyceridaemic patients and in normal men.

In six patients with hypertriglyceridaemia presenting whilst receiving treatment with beta-adrenoreceptor blocking drugs (mean serum triglycerides 31.2 mmol/l) the half-life (t1/2) of an intravenously administered triglyceride emulsion was 32.8 +/- 7.9 min (mean +/- SEM) on beta-blocker and 22.8 +/- 4.8 min after stopping beta-blocker treatment. In three of these patients subsequent administration of a beta-blocker with intrinsic sympathomimetic activity had no effect on t1/2. In a cross-over trial of placebo, atenolol (beta 1-blocker), propranolol (beta 1- and beta 2-blocker) and pindolol (beta 1- and beta 2-blocker with intrinsic sympathomimetic activity) in 11 normal men t1/2 was 11.8 +/- 0.9, 12.6 +/- 1.1, 14.3 +/- 1.7 and 12.4 +/- 1.1 min respectively. None of the apparent differences achieved statistical significance, but in two men marked increases in t1/2 occurred on propranolol. The concentrations of serum triglycerides and very low density lipoprotein cholesterol in the normal men were, however, increased by beta-blockade, most markedly by pindolol. Serum high density lipoprotein (HDL) cholesterol concentration decreased in normal men on beta-blockers, most clearly on atenolol and propranolol. This decrease was due to a reduction in cholesterol in the HDL2 subfraction. No statistically significant effects on serum low density lipoprotein cholesterol or apolipoprotein B concentrations occurred in the normal men. The doses of atenolol and propranolol used in this study were equipotent as judged by the heart rate response to exercise.

Adrenergic beta-Antagonists↗
PubMed1988

Beta 2-sympathomimetic activation as a cause of posthypoglycemic glucose intolerance.

Posthypoglycemic glucose intolerance is related to counter-regulatory hormones. We have tested the role of the beta 2-sympathomimetic activity of the catecholamines in healthy volunteers. beta 2-stimulation with fenoterol for 25 minutes caused glucose intolerance and insulin resistance for 4 hours. This suggests that the beta 2-sympathomimetic activity induces glucose intolerance after an episode of hypoglycemia.

Blood Glucose↗
PubMed1986

Effects of beta blocking agents on the density of beta adrenoceptors and adenylate cyclase response in human myocardium: intrinsic sympathomimetic activity favours receptor upregulation.

The density of beta adrenoceptors, the relative number of beta 1 and beta 2 adrenoceptor subtypes, and adenylate cyclase activity were studied in preparations from atrial biopsy specimens of 32 patients with coronary heart disease. Six patients were not receiving beta blocking agents, whereas the others were treated with different beta blocking drugs (timolol, propranolol, pindolol, metoprolol, and atenolol). Clinical and haemodynamic variables were similar in the different groups of patients. Beta adrenoceptor density was 17% significantly lower in the non-treated group than in the groups treated with beta blocking drugs. Among these, the group treated with pindolol, a drug with intrinsic sympathomimetic activity, had receptor densities that were 38% significantly higher than those treated with other beta blocking drugs and 51% significantly higher than the non-treated group. The relative numbers of beta 1 and beta 2 adrenoceptor subtypes were very similar in the different groups (beta 1 receptors 75-80%, beta 2 receptors 20-25%). A significant increase in the ratios of terbutaline stimulated to basal and terbutaline stimulated to isoproterenol stimulated adenylate cyclase activities was found in patients treated with beta 1 selective blockers (metoprolol, atenolol), indicating that beta 1 selective drugs may improve beta 2 receptor-adenylate cyclase coupling. In contrast, pindolol caused a significant reduction in the ratio of terbutaline stimulated to isoproterenol stimulated adenylate cyclase activity, indicating that this drug may cause a reduction in beta 2 receptor-adenylate cyclase coupling efficacy. Thus treatment with beta blocking agents causes upregulation of human myocardial beta receptor density. Intrinsic sympathomimetic activity seems to favour receptor upregulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗
PubMed1978

Compartmental shift of potassium--a result of sympathomimetic overdose.

A 17-year-old youth was admitted with a serum potassium concentration of 1.8 mmol/l after taking an overdose of pseudoephedrine and choline theophyllinate. Apart from tachycardia, tachypnoea and ankle clonus, examination was normal as was the initial electrocardiograph. The hypokalaemia resolved, but there was an overall positive potassium balance of only 13 mmol. This suggests that the sympathomimetics provoked a compartmental shift of potassium perhaps indirectly by inducing hyperglycaemia and hyperinsulinaemia, as well as directly. Other factors known to affect body potassium distribution were excluded. The fact that features commonly associated with hypokalaemia could not be demonstrated may be explained by a normal body potassium content. Severe hypokalaemia caused by a compartmental shift occurs with large doses of sympathomimetics as well as in periodic paralysis.

Adolescent↗
PubMed1978

Metabolic effects of beta-sympathomimetic drugs and dexamethasone in normal and diabetic pregnancy.

Marked hyperglycaemia and hyperinsulinaemia were observed in two normal women in premature labour treated with an intravenous infusion of a beta-sympathomimetic drug and intramuscular dexamethasone injections. Similar therapy in a chemical diabetic patient caused diabetic ketoacidosis, while treatment of an insulin dependent diabetic with dexamethasone alone resulted in a major increase in her insulin requirements. It is suggested that the diabetogenic effects of beta-sympathomimetic drugs and dexamethasone may be additive and that regular plasma glucose estimations should be made when they are used, especially in patients with impaired glucose tolerance.

Adolescent↗
PubMed1977

Potentiation of beta-sympathomimetics with alpha-adrenoceptor blocking drugs in guinea pig trachea and human bronchus preparations.

The actions of beta-sympathomimetics alone and in various combinations with alpha-adrenoceptor blocking agents were studied in guinea pig tracheal chain and in some preparations of human bronchi taken in operations. All the alpha-adrenoceptor blockers caused 50-100% potentiation of the effects of the beta-sympathomimetics studied in both preparations, had no effects of their own in the rather low concentrations used (10(-10) --10(-6) mol/l). The results show that guinea pig and human tracheobronchial smooth muscle react similarly to these drugs and may contain adrenergic alpha-receptors.

Adrenergic alpha-Antagonists↗
PubMed1978

A brief review of sympathomimetic bronchodilators and a description of a new selective agent, rimiterol hydrobromide.

The development of beta2-specific sympathomimetic bronchodilators (rimiterol, salbutamol, terbutaline) has made the basic treatment of asthmatic patients more safe and effective. Despite that, the asthmatics should be under careful control and all patients should be taught the correct way to use their bronchodilator aerosols. If a sympathomimetic drug has lost its effectiveness, the patient should be able to have easy contact to the treating physician or outpatient department.

Adrenergic beta-Agonists↗
PubMed1991

Effect of halothane on arrhythmogenic responses induced by sympathomimetic agents in single rat heart cells.

The combination of catecholamines and halothane has long been recognized as arrhythmogenic. The purpose of this study was to evaluate whether the mechanism of this interaction originates at the single cell level. The incidence of spontaneous contractile waves occurring between stimulated beats (interbeat waves), early aftercontractions, and late aftercontractions was measured in rat myocytes exposed to sympathomimetics with and without halothane. Each of these endpoints in single cells has the potential to produce arrhythmias in multicellular preparations. Interbeat waves and late aftercontractions were observed with isoproterenol (1 X 10(-7) M) and norepinephrine (1-3 X 10(-7) M). The incidence of these phenomena was significantly reduced in the presence of 0.30 mM halothane. Early aftercontractions occurred in the presence of isoproterenol (1 X 10(-7) M), norepinephrine (1-3 X 10(-7) M), and phenylephrine (5-10 X 10(-6) M). There was a statistically significant decrease in the incidence of early aftercontractions in the presence of 0.30 mM halothane. These results indicate that the mechanism behind the clinically observed increased arrhythmogenicity of catecholamines with halothane does not arise at the level of single ventricular cells because halothane inhibited sympathomimetic-induced arrhythmogenic activity in this model. The probable mechanisms rather include altered impulse propagation, which might lead to phenomena such as reentry.

Animals↗
PubMed1976

alpha-Adrenoceptors mediating positive inotropic effects on the ventricular myocardium: some aspects of structure-activity relationship of sympathomimetic amines.

Experiments were carried out on the isolated papillary muscle of the rabbit in order to further characterize the alpha-adrenoceptors mediating the positive inotropic effect. For this purpose dose-response relations of seven sympathomimetic amines were compared under the influence of alpha- and/or beta-adrenolytic drugs. Phentolamine (10(-6) M) shifted the lower part of the dose-response curves for norfenephrine, synephrine and epinine as for phenylephrine and adrenaline to the right, while prindolol (10(-8) M) affected only the upper part of the curves. In the presence of both alpha- and beta-adrenoceptor blocking agents the entire dose-response curves for sympathomimetic amines were shifted in a parallel manner. Noradrenaline affected preferentially beta-adrenoceptors, whereas its effect on alpha-adrenoceptors was so weak that it could be detected only when the neuronal and extraneuronal uptake mechanism of amines were blocked by cocaine (3 X 10(-5) M) and corticosterone (4 X 10(-5) M), respectively. The effect of dopamine was not affected either by phentolamine or by prindolol, but was antagonized by the simultaneous application of both alpha- and beta-adrenoceptor blocking agents. From the present results, it appears that the following relationships are present between the structure of amines and the alpha-adrenoceptor stimulating activity in the heart: (1) N-methylation increases the potency: (2) Absence of the hydroxyl group either in 3 or in 4 position decreases the intrinsic and beta-adrenoceptor stimulating activities, but increases the alpha-adrenoceptor stimulating activity.

Adrenergic alpha-Agonists↗
PubMed1992

Intravenous propranolol reverses hypertension after sympathomimetic overdose: two case reports.

Hypertension is a potential complication following ephedrine and pseudoephedrine overdoses. Treatment with propranolol, a beta blocker, is not recommended since it may produce be an alpha agonist with the potential for further elevated blood pressure. Two patients who developed hypertension following sympathomimetic overdoses were treated with propranolol. After ingesting 4500 mg of pseudoephedrine, a 24 year-old male developed a blood pressure of 220/108. Five min after intravenous propranolol 1 mg BP was 153/88. After ingesting 17,500 mg of ephedrine a 29 year-old female developed a BP of 168/106. Her BP was 124/90 five min after intravenous propranolol. Further study is needed to investigate the potential therapeutic benefit of propranolol in the treatment of sympathomimetic-induced hypertension.

Adult↗
PubMed1975

An analysis of the sympathomimetic activity of 6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline (TIQ).

The pithed rat preparation has been used to study the sympathomimetic activity of 6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline (TIQ). In this preparation, an increase in blood pressure is indicative of alpha stimulation, and an increase in heart rate is indicative of beta stimulation. Using this preparation, we have found that TIQ is approximately 3 orders of magnitude less potent than norepinephrine in evoking changes in blood pressure and heart rate. The activity of TIQ has also been studied in pithed animals which had been previously sympathectomized with 6-hydroxydopamine. Sympathectomy produced a marked reduction in cardiac norepinephrine, and it nearly abolished vascular responses to injected tyramine. Following sympathectomy, pithed animals were supersensitive to norepinephrine and subsensitive to TIQ. Similar results were obtained on pithed animals that had been pretreated with cocaine. It is concluded that TIQ is a weak sympathomimetic agent possessing both directly and indirectly acting properties. The data are discussed in terms of a proposal that TIQ may be a false adrenergic transmitter.

Adrenergic alpha-Agonists↗
PubMed1990

[Ocular side effects of added sympathomimetics in local anesthetics].

In facial dermatosurgery, the addition of sympathomimetics to local anesthetics produces a desirable topical effect as they provide an almost bloodless operation field due to temporary vasoconstriction. In an 87-year-old woman, who had lost her left sight owing to a meningoma, we removed a basal-cell carcinoma from the right side of her nose. The local anesthetic applied contained noradrenaline at a concentration of 1:50,000. After the operation, the patient complained of a headache and a transitory loss of sight. We suppose that noradrenaline reached the arteria centralis retinae via arterial periorbital anastomoses, thus causing a vasoconstriction of this artery. As far as dermatosurgery of the middle and upper face is concerned, patients with severe vision disorders should be considered as a risk group; in local anesthesia of those patients an addition of sympathomimetics should be avoided.

Aged↗
PubMed1987

Acute hemodynamic and neurohumoral effects of pindolol: a beta-adrenoceptor antagonist with high intrinsic sympathomimetic activity in patients with dilated cardiomyopathy.

It has been claimed that beta-adrenoceptor antagonists produce clinical improvement and increase longevity in patients with idiopathic dilated cardiomyopathy. Dilated heart is critically dependent upon adrenergic support to maintain forward output. Acute withdrawal of such support, even with small doses of beta-blockers, may worsen myocardial function sufficiently to limit their widespread use. Pindolol (P), a potent beta-adrenoceptor antagonist, possesses high intrinsic sympathomimetic activity. Administration of P to patients with dilated cardiomyopathy may protect against the effects of high circulating catecholamines and at the same time partially maintain intrinsic left ventricular function. We examined the acute hemodynamic effects of P (2.5 mg orally) in seven patients with dilated cardiomyopathy (average ejection fraction, 23%) and resting tachycardia (average, 111 beats/min). As compared to baseline values, P produced a highly significant fall in heart rate (rest, 19%, p less than 0.001; exercise, 24%, p less than 0.01), cardiac output (rest, 20%, p less than 0.01; exercise, 25%, p less than 0.001), and systemic arterial pressure (exercise only, 13%, p less than 0.05). Calculated systemic vascular resistance increased significantly at rest (17%, p less than 0.05). Pulmonary artery pressures did not change. Compared to normal subjects, baseline norepinephrine levels were markedly elevated in patients with dilated cardiomyopathy at rest and during exercise. Pindolol produced a further significant increase in norepinephrine levels. Two of seven patients became appreciably short of breath after P. Despite its substantial intrinsic sympathomimetic activity, pindolol, like other beta-adrenoreceptor antagonists, produces significant hemodynamic impairment in patients with congestive cardiomyopathy. An exaggerated norepinephrine response after the drug may, by increasing peripheral vascular resistance, lead to further deterioration in left ventricular performance.

Adult↗
PubMed1987

The influence of castration and antiandrogenic treatment on the sensitivity of rat seminal vesicle to sympathomimetic drugs.

The sensitivity of seminal vesicles to sympathomimetic drugs and the plasma concentrations of testosterone and gonadotropins (LH and FSH) were examined in adult male albino rats divided into three groups: normal, castrated and Androcur-treated. Dose-effect curves for adrenaline and noradrenaline were obtained in the presence and absence of cocaine or corticosterone and the parameter pD2 was determined. Castration and Androcur treatment induced a decrease in seminal vesicle sensitivity to drugs (shifting of dose-effect curves to the right, decreased pD2). Cocaine shifted the adrenaline and noradrenaline dose-effect curves to the left in three groups. Corticosterone did not modify the dose-effect curves of adrenaline and noradrenaline. Plasma testosterone levels were decreased by castration and Androcur-treatment although the LH and FSH concentrations were markedly altered by castration but were unaltered by the antiandrogenic treatment. The results suggest that the androgen may play an important role in the sensitivity of the seminal vesicle to sympathomimetic drugs through control of the neuronal uptake of catecholamines.

Androgen Antagonists↗
PubMed1986

The treatment of acute transient cough: a placebo-controlled comparison of dextromethorphan and dextromethorphan-beta 2-sympathomimetic combination.

The efficacy of an antitussive-beta 2-sympathomimetic combination (dextromethorphan-salbutamol) was compared with that of a plain antitussive (dextromethorphan) and a placebo in a double-blind trial in 108 out-patients with cough associated with acute respiratory infection. The dextromethorphan-salbutamol combination was superior to dextromethorphan or placebo in the suppression of cough at night, although a spontaneous improvement occurred in all treatment groups during the 4-day treatment period. No statistically significant differences between the treatments were shown in the symptom scores for the cough frequency and severity during the day, sputum quantity or ease of expectoration. A significant improvement in cough during the day was observed in all treatment groups. The results suggest that the use of antitussives is usually unnecessary; the only indication might be symptomatic relief, especially at night. An antitussive combined with a beta 2-sympathomimetic might be the most effective treatment in this type of cough.

Acute Disease↗
PubMed1978

[The harmful effects of beta2-sympathomimetic drugs as uterine relaxants on caesarean section (author's transl)].

Beta2-sympathomimetics are the most powerful inhibitors of uterine contraction used in order to prevent threatening fetal asphyxia. These drugs, however, can cause harmful interactions with anaesthetics during caesarean section. Our patient-material consists of parturients, who were given a beta2-sympathomimetic, ritodrine, immediately before caesarean section performed under combined general anaesthesia. These patients showed significantly more marked tachycardia, hypotonia and abundant haemorrhage during operation as a consequence of poor uterine contractility than did the control group. Rapid variations in the circulation of the mother may also be disadvantageous to the wellfare of the fetus. These side-effects can best be minimized by omitting atropine-premedication and by expanding the blood volume of the mother before caesarean section with adequate infusion of Ringer-type.

Adult↗
PubMed1994

[Long-term effect of the beta 2-sympathomimetic formoterol in young smokers--study of duration and site of effect of bronchodilatation using conventional methods of lung function and monodispersed aerosols].

Formoterol is a novel selective beta 2-sympathomimetic inducing bronchodilatation after inhalation or oral application. Compared to other beta 2-sympathicomimetics the substance begins to act very rapidly even at a much lower dosage level, while it remains effective for at least 12 hours. In the present study the bronchodilatory effect of 24 micrograms MDI formoterol was investigated in 18 healthy smokers between 20 and 30 years of age means. Measurement was effected by means of conventional lung function diagnostics (body plethysmography, spirometry) and an biophysical aerosol measurement method for determining the effective airways dimensions (EAD). This method is based on the gravitational losses of a previously inspired monodisperse model aerosol during apnoea periods of different duration. It enables determination of the EAD as a function of the volumetric lung depth (VLT). A marked and universally measurable bronchodilatation is detectable directly after formoterol has been inhaled. The longterm action of formoterol was confirmed for more than 15 hours after application, using the conventional lung function test and the EAD method. Over and above this the EAD determination showed that the bronchodilatory effect was much more marked in the central airways than in the periphery of the lungs, thus confirming the effect generally described for beta 2-sympathomimetics as being mainly directed towards the central airways region.

Administration, Inhalation↗
PubMed1998

Induction of atypical prostatic hyperplasia in rats by sympathomimetic stimulation.

BACKGROUND: Prostatic innervation may participate in its homeostasis and growth. alpha-Adrenergic inhibition alleviates clinical symptoms in benign prostatic hyperplasia. However, the prostatic effect of adrenergic agonists has not been investigated. This study deals with the prostatic effect of subchronic sympathomimetic stimulation. METHODS: Male rats received daily subcutaneous injections of the alpha-adrenergic agonist phenylephrine, 1, 10, or 20 mg/kg per day, the beta-adrenergic agonist isoproterenol, 1, 2.5 or 5 mg/kg per day, or saline, for 30 days, and the prostates were removed for histopathological examination. RESULTS: Phenylephrine induced atypical prostatic hyperplasia, characterized by piling-up with papillary and cribriform patterns, and budding-out of epithelial cells. It decreased prostatic secretions and total weight. Similar results were observed in orchidectomized rats receiving exogenous testosterone supplementation. Isoproterenol had no prostatic morphological effect. CONCLUSIONS: These results raise the possibility that sympathetic stimuli play a role in normal and aberrant growth and differentiation of prostatic epithelium, and suggests neurostimulants-treated animals as a model to study the etiology and development of prostatic hyperplasia.

Adrenergic alpha-Agonists↗