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At least 163 records · Page 9Linked to original sources

PubMed1981

Sympathomimetic and cardiodepressant effects of acebutolol, oxprenolol, pindolol, and propranolol. A comparative study on changes in hemodynamics, contractility, heart rate, and AV-conduction time at therapeutic doses.

The present study was undertaken in order to obtain further informations on non-beta-antiadrenergic properties of the four beta-sympatholytic agents acebutolol, oxprenolol, pindolol, and propranolol. Standardized experiments were performed using a chronically reserpinized canine preparation for the assessment of dose-response curves of changes in hemodynamics, left ventricular contractility, heart rate, AV-conduction time, and myocardial oxygen consumption especially at therapeutic doses. Our results show that acebutolol and oxprenolol, at doses clinically recommended, exert moderate positive inotropic effects but do not influence heart rate significantly. Pindolol has a strong both positive chronotropic and inotropic efficacy, even at small therapeutic doses. Propranolol produces neither chronotropic nor inotropic effects. In contrast to the literature acebutolol exerts direct cardiodepression at doses clinically used, whereas oxprenolol, pindolol, at propranolol have no direct cardiodepressant properties at those doses. Thus the relationship between the dose requirements for chronotropic and inotropic sympathomimetic effects differs for each beta-sympatholytic agents, and in may prove impossible to get an order of intrinsic sympathomimetic potency of beta-blockers comparing dose-response curves of heart rate changes only. As shown in the case of acebutolol, direct cardiodepression of beta-sympatholytic agents may occur at therapeutic doses.

Acebutolol↗

PubMed1984

Effects of sympathomimetic drugs on reptilian atrial muscles.

The effects of some sympathomimetic drugs on isolated atria of rainbow lizards (Agama agama Linn.) and land tortoises (Kinixys spp. Linn.) have been examined. Noradrenaline, adrenaline, isoprenaline, phenylephrine or dopamine (10(-9)-10(-5) M) induced concentration-dependent positive chronotropic and inotropic responses in spontaneously-beating right- and electrically-driven left atria of rainbow lizards or tortoises. These catecholamines produced similar responses in guinea-pig isolated atria. Phentolamine or propranolol (10(-10)-10(-6) M) competitively antagonised the positive chronotropic and/or positive inotropic responses induced by these sympathomimetic agonists in these reptilian (and mammalian) atrial muscles; probably suggesting the presence of alpha- and/or beta-adrenoceptors in reptilian atrial muscles (as in the mammalian myocardium). It is suggested that in reptilian atrial muscles, only one adrenoceptor subtype which is capable of converting its properties to either alpha- or beta-, or even alpha- and beta-adrenoceptor subtypes (as in the frog heart) depending on the environmental temperature, may exist. The use of rainbow lizard and tortoise atrial muscle preparations as laboratory models for routine pharmacological evaluation of adrenergic drugs, particularly in developing tropical African countries where these cheap, harmless reptiles abound, is strongly recommended.

Animals↗

PubMed1984

Fasting reduces the responses of the rat vas deferens to sympathomimetics.

The effect of fasting, L-DOPA pretreatment and high glucose medium on the response of the rat vas deferens to sympathomimetics was studied in vitro. The contractile responses of the rat isolated vas deferens were reduced by fasting, the effect being significant after 24-hr fast with noradrenaline and tyramine, after a 48-hr fast with dopamine, and after a 72-hr fast with methoxamine. Treatment with L-DOPA for 7 days before sacrifice abolished the effect of a 24-hr fast in reducing responses to noradrenaline and tyramine, and the response to methoxamine after a 72-hr fast was enhanced. Doubling the concentration of glucose in the solution bathing the isolated vas deferens from rats fasted for 24 hr increased the responses to noradrenaline and tyramine. It is concluded that fasting reduces the responses of the rat vas deferens to sympathomimetics whilst L-DOPA pretreatment and high glucose restore and/or enhance the responses.

Animals↗

PubMed1980

Metiamide potentiates the stimulant actions of sympathomimetic amines "in vitro".

Metiamide significantly potentiated the contractions of the guinea-pig and the rat vas deferens and seminal vesicle produced by noradrenaline, dopamine and methoxamine. The responses to acetylcholine and carbachol were not affected by metiamide. Tetrodotoxin did not affect metiamide-induced potentiation of the sympathomimetics. Potentiation induced by metiamide was Ca++-dependent. Mepyramine failed to influence the responses to the amines. It is suggested thaat extra-neuronal mechanisms may be involved in the interactions of metiamide and sympathomimetics.

Acetylcholine↗

PubMed1982

[Sympathomimetic drugs in the treatment of childhood asthma].

Sympathomimetic bronchodilators relax bronchial smooth muscle via stimulation of the enzyme adenylcyclase. Furthermore, they stabilize the membrane of the bronchial mast cell. Therefore, they are used in the treatment of acute asthma as well as in long-term prophylaxis. A new generation of beta 2-receptor binding derivates of isoproterenol offers increased therapeutic safety because of a reduced risk of cardiovascular side effects. Three routes of medication are available. Parenteral therapy is reserved for the treatment of acute severe asthma. The oral route can be used for long-term medication in smaller children. Mist therapy offers the advantage of topic medication. Efficient handling of a metered-dose aerosol is beyond the capabilities of small children; these patients get their topic treatment by nebulized solutions. The relevant data of clinical pharmacology are summarized for all forms of medication. Focusing on the role of sympathomimetic drugs, a medication strategy for the treatment of acute asthma as well as for long-term prophylaxis is described.

Administration, Oral↗

PubMed1981

[Arterial hypertension due to abuse of sympathomimetic drugs. One case (author's transl)].

A 36-year-old woman developed severe arterial hypertension after taking for five consecutive years increasing dose (up to 10 mg per day) of phenoxazoline HCl in nasal spray. A relationship between the abuse of this sympathomimetic drug and the hypertension was suggested by the unusual appearance of renal arteries on arteriography (stenosis and dilatations resembling aneurisms), the increase in renin activity and the disappearance of hypertension after the drug was discontinued. On control examination, two years later, blood pressure, renin activity and renal arteries were normal. The possibility of sympathomimetic drug overdosage must be borne in mind in cases of suspected iatrogenic arterial hypertension.

Adult↗

PubMed1976

The adsorption of sympathomimetic agents by activated carbon hemoperfusion.

Sympathomimetic agents with mixed and pure alpha and beta adrenergic activity are adsorbed by coconut shell activated carbon from blood, sufficiently rapidly to markedly reduce the activity of these agents. The results of this study suggest that the site of injection of sympathomimetic agents being considered for correcting hypotension during activated carbon hemoperfusion be selected to permit systemic mixing before circulation into the adsorption device.

Adsorption↗

PubMed1987

Effects on physical performance of intrinsic sympathomimetic activity (ISA) during selective beta 1-blockade.

In 15 healthy, not specifically trained volunteers (age: 26.6 +/- 2.7 years) single equipotent doses of a selective beta 1-blocker with intrinsic sympathomimetic activity (ISA) (200 mg Epanolol-Visacor; V) and of a selective beta 1-blocker without ISA (100 mg Metoprolol; M) were compared with placebo (P) with respect to their influence upon physical performance capacity and metabolism in a random, double blind, cross-over experimental setting. The subjects underwent three step by step incremental treadmill tests and three treadmill endurance tests until volitional exhaustion. Maximum running speed and maximum oxygen uptake were used as measures of maximum performance capacity. Running speed and oxygen uptake related to individual anaerobic threshold, and running time and running distance in the endurance tests were used as measures of endurance capacity. Both maximum and endurance performances were reduced significantly by beta-blockade. No relevant differences were discerned between V and M. The uniform reduction in exercise heart rate with both beta-blockers demonstrated the application of equipotent doses. At rest, heart rate was significantly higher under V than under M. Carbohydrate metabolism was unaffected, both beta-blockers showing equal inhibition of lipolysis during exercise. We conclude that intrinsic sympathomimetic activity has no influence upon physical performance and metabolism during selective beta 1-blockade.

Adrenergic beta-Antagonists↗

PubMed1980

The effects of beta-sympathomimetic amines and phosphodiesterase inhibitors on electrophysiological parameters in Purkinje fibres.

Dose-dependent responses to L-isoprenaline of spontaneous activity and plateau height in Purkinje fibres can be mimicked closely by the PDE-inhibitor IBMX. Simultaneous applications of sympathomimetic amines and IBMX result in potentiated responses. The results support the hypothesis that cyclic-AMP is the common mediator of positive chronotropic and inotropic effects induced by beta-sympathomimetic amines.

1-Methyl-3-isobutylxanthine↗

PubMed1984

Apparent superiority of H2-receptor stimulation and simultaneous beta-blockade over conventional treatment with beta-sympathomimetic drugs in post-acute myocardial infarction: cardiac effects of impromidine--a new specific H2-receptor agonist-in the surviving catecholamine-insensitive myocardium.

Left ventricular infarction (AMI) was produced in experimental animals and the contractile response to beta-adrenergic and H2-histaminergic stimulation by isoproterenol and impromidine tested in the isolated perfused heart preparation. Adenylate cyclase activity as well as binding characteristics of [3H]-dihydroalprenolol ([3H]-DHA), [3H]-methyl-tiotidine ([3H]-TIOT) and [3H]-quinuclidinyl benzilate ([3H]-QNB) to cardiac beta 1-, H2- and cholinergic muscarinic receptors were determined in sarcolemmal membrane preparations of the right ventricle of the same hearts. In addition, an attempt was made to elucidate the therapeutic value of post-AMI treatment with impromidine in the presence and absence of beta-blockade, in contrast to administration of prenalterol and the conventional therapy with beta-sympathomimetic drugs, e.g. dobutamine. Three days post-AMI the dose-response curve for isoproterenol of right ventricular dP/dtmax was significantly depressed, while the inotropic effect of impromidine was not impaired. Stimulation of adenylate cyclase activity by isoproterenol was reduced by 80% whereas impromidine and NaF stimulation rates were unaltered. Receptor-binding studies indicated a 90% loss and 10-times lowered affinity (KD) of the remaining beta-receptors while specific [3H]-TIOT- and [3H]-QNB-binding was unchanged. Administration of dobutamine increased mortality rates and extension of infarct size, led to a further decrease in contractile response to isoproterenol, induced complete insensitivity of adenylate cyclase to isoproterenol stimulation and caused pronounced additional reduction of number and affinity of [3H]-DHA-binding sites. In contrast, all above alterations were prevented by treatment with either prenalterol or combined administration of impromidine plus metoprolol. It is concluded, that these alterations in the non-ischemic, uninvolved myocardium post-AMI are the result of catecholamine-induced specific damage of sarcolemmal beta-receptors. Furthermore, treatment with H2-agonists in combination with beta-blocking agents may have beneficial effects, whereas conventional therapy with beta-sympathomimetic drugs tends to worsen the already depressed function of the beta-adrenergic stimulation mechanism.

Adenylyl Cyclases↗

PubMed1979

[Investigations of the effect and mechanism of action of the beta-sympathomimetic ritodrine on the synthesis and release of dipalmitoyl-lecithin in the fetal rabbit lung (author's transl)].

For a period of 8 days, pregnant white New Zealand rabbits were treated either with the beta-sympathomimetic Ritodrine (1 mg/kg) body weight daily) or with 0.9% saline solution. The fetuses were delivered by caesarian section on the 25th and 30th day of gestation (term being 31 days). No significant difference was found between the Ritodrine and saline treated groups with respect to the levels of dipalmitoyl-lecithin (DPL) obtained from the homogenates as well as the alveolar lavages of the fetal lungs. These results indicate that with this experimental model, prepartum treatment with Ritodrine has no effect either on DPL synthesis or its release into the alveolar spaces. Furthermore, treatment with the beta-sympathomimetic produced no significant change in the concentrations of the specific glucocorticoid receptors in the cytosol and nuclei of the fetal lungs, and in addition, the lung cytosol glucose concentrations as well as the plasma corticosteroid levels were unaffected. These findings support the conclusion that the synthesis of DPL in the fetal lung is not stimulated by Ritodrine.

Animals↗

PubMed1981

Redistribution of myocardial blood flow distal to a dynamic coronary arterial stenosis by sympathomimetic amines: comparison of dopamine, dobutamine and isoproterenol.

The effects of dopamine, dobutamine and isoproterenol on coronary hemodynamics, severity of stenosis, distal bed resistance and transmural myocardial perfusion gradients with radioactive microspheres were studied in dogs with a mild obstruction of the left circumflex coronary artery anesthetized with morphine-chloralose. Changes in transmural blood flow were related to the ratio of the diastolic aortic pressure-time index to tension-time index (DPTI/TTI) and the ratio of the distal diastolic coronary pressure-time index to tension-time index (DDPTI/TTI). At doses of 5 microgram/kg per min, dopamine had no significant effect on DPTI/TTI, DDPTI/TTI or endocardial/epicardial flow ratio; however, dobutamine produced a slight decrease in this flow ratio and in DDPTI/TTI. At doses of 10 microgram/kg per min, both drugs produced a significant (p less than 0.05) reduction in diastolic coronary pressure distal to the stenosis. DDPTI/TTI and endocardial/epicardial flow ratio without change in DPTI/TTI. In comparison, isoproterenol (0.01 and 0.05 microgram/kg per min) produced dose-related decreases in endocardial/epicardial flow ratio, DDPTI/TTI and DPTI/TTI. During infusion of each sympathomimetic agent, there was a corresponding reduction in distal bed vascular resistance but a concomitant increase in stenosis resistance. The results also show that dopamine and dobutamine, as well as isoproterenol, area capable of producing a maldistribution of coronary blood flow distal to a mild coronary arterial stenosis and that such a redistribution of glow is dependent on dose, reduction of the distal diastolic coronary pressure-time index and decrease in DDPTI/TTI. It is further concluded that hemodynamic changes distal to a coronary arterial stenosis seriously jeopardize the usefulness of DPTI/TTI; however, DDPTI/TTI can be used to predict drug effects on the endocardial/epicardial flow ratio in an ischemic area. This study demonstrates that "fixed" stenoses can undergo dynamic processes and sympathomimetic amines increase the resistance to flow through a stenotic coronary artery in the nonfailing heart.

Animals↗

PubMed1991

Long-acting alpha 1-adrenoceptive sympathomimetic agent suppresses sympathetic outflow to muscles in humans.

To clarify the effect of a long-acting selective alpha 1-adrenoceptive sympathomimetic agent on sympathetic outflow to muscles (muscle sympathetic activity, MSA) in humans, 5 mg of midodrine hydrochloride was injected intravenously in ten healthy male subjects aged 19-25. Spontaneous MSA was significantly suppressed as well as plasma norepinephrine level without changing heart rate, or systemic blood pressure. The suppression continued for more than 90 min, and this is supposed to be due to negative feedback action on the baroreflex loop. The absence of significant changes in heart rate or systemic blood pressure in healthy subjects suggests that hemodynamic homeostasis is maintained by reducing the MSA in response to a long-acting sympathomimetic agent, like midodrine hydrochloride, which constricts peripheral vessels directly.

Adrenergic alpha-Agonists↗

PubMed1984

Effect of beta blockade and intrinsic sympathomimetic activity on exercise performance.

Beta-adrenergic receptor blocking drugs with intrinsic sympathomimetic activity may have the advantage of not depressing myocardial function and pulse rate at rest. Little is known about their effects during exercise. Thus, the effects of small and large doses of pindolol, a nonselective beta-adrenergic blocking drug with intrinsic sympathomimetic activity, were compared with the effects of small and large doses of propranolol in 13 normal men during treadmill exercise. Compared with placebo, all drug regimens decreased exercise duration (p less than 0.001). There were no significant differences in duration between pindolol and propranolol, or between the small and large dose of each drug. Maximal oxygen consumption tended to be lower with all preparations compared with placebo (p less than 0.10). With smaller doses, decrements of maximal heart rate (HR) and HR-blood pressure (BP) product were equivalent for pindolol and propranolol (decreases of 46 vs 43 beats/min, and 13,000 vs 12,000 units). The HR-BP product decreased more with high-dose propranolol than high-dose pindolol (decrease of 18,000 vs 14,800 units) due to a greater decrement in HR with propranolol (decrease of 65 +/- 3 vs 53 +/- 3 beats/min). At both submaximal levels, for both low- and high-dose preparations, HR, BP and HR-BP product were lower for propranolol than for pindolol. Thus, in healthy subjects, pindolol and propranolol at doses that produced equivalent reductions in maximal oxygen consumption, exercise duration and, for the smaller dose, HR, had different effects on submaximal HR-BP product, an index of myocardial oxygen consumption, as a result of a higher HR and BP with pindolol.

Adult↗

PubMed1985

Continuous long-term intravenous beta-sympathomimetic tocolysis.

This report concerns the clinical course and outcome of 16 patients treated by continuous long-term intravenous beta-sympathomimetic tocolysis (greater than or equal to 1 week's intravenous therapy). Half of the patients received such therapy for at least 5 weeks. Intravenous tocolysis was adjusted to decrease uterine activity and maintain a satisfactory pulse and blood pressure. Parenteral tocolysis was continued until there was a successful transition to oral therapy, until fetal maturity, or until maternal/fetal indications for delivery were noted. Data indicate that the cardiovascular and metabolic effects were pronounced mostly during the first 3 to 4 days of therapy and then returned toward pretreatment values. In none of the study patients was the treatment discontinued because of drug-related problems, electrocardiogram changes, chorioamnionitis, or fever. The experience indicates that, in a selected group of patients and under close supervision, continuous long-term intravenous beta-sympathomimetic tocolysis may be considered a safe therapeutic modality able to prolong pregnancy with a more desirable outcome.

Administration, Oral↗

PubMed1979

Neonatal hypoglycemia after beta-sympathomimetic tocolytic therapy.

The effect of oral beta-sympathomimetic tocolytic therapy on neonatal serum glucose concentrations in the first several hours after delivery was examined in 12 babies. Hypoglycemia was noted in eight babies, and was sustained over at least a 30-minute period in five. The group with sustained hypoglycemia had a higher cord serum insulin concentration, a lower serum glucose nadir, and a more rapid initial rate of serum glucose disappearance than those babies with normoglycemia or transient hypoglycemia. Sustained hypoglycemia was observed in five of six babies delivered within two days of the termination of tocolytic therapy, but was not present in any of six babies delivered five or more days after the end of tocolytic therapy. Speculations as to the interaction between beta-sympathomimetic tocolytic drugs administered to the mother and fetal and neonatal glucose metabolism are made.

Ethanolamines↗

PubMed2001

A possible indirect sympathomimetic action of metformin in the arterial vessel wall of spontanously hypertensive rats.

The antidiabetic drug metformin (MF) typically achieves only micromolar levels in plasma with normal therapeutic use. However, it is also known to accumulate in various tissues up to several times higher after standard oral dosing and we now have evidence from both in vivo and in vitro experiments with spontaneously hypertensive rats (SHR) that millimolar levels stimulate release of norepinephrine (NE) from vascular sympathetic nerve endings (SNEs). As shown in the present work with SHR tail arterial tissue (rich in SNEs), the known vasodilator effect of millimolar levels of MF on the smooth muscle (even if contracted with a nonadrenergic agonist), is attenuated by the presence of the SNEs unless phentolamine (an alpha receptor blocker) is present. We reasoned that the mechanism for this apparent NE-releasing action of MF is not exocytotic release as that would require depolarization of the neuronal cell membranes in SNEs, and MF at millimolar levels is known to repolarize (not depolarize) membranes of other cells. Thus, we tested the possibility that MF releases NE by an indirect sympathomimetic-like action. Such an action should be amplified by monoamine oxidase inhibitors (e.g. iproniazid) and blocked by NE-carrier inhibitors (e.g. desipramine). Accordingly, we found that the abovementioned attenuating effect of intact SNEs on MF's relaxation of SHR tail arterial tissue (compared to tissues in which SNEs were experimentally removed with 6-hydroxydopamine) was amplified nearly 3-fold by iproniazid (p<0.05) and blocked by desipramine (p<0.05). These results support an indirect sympathomimetic action of MF and raise the question whether commonly used antidepressants with properties similar to iproniazid and desipramine might alter MF's beneficial vasodilatory (and thus antihypertensive) effectiveness in diabetic patients with hypertension.

Animals↗

PubMed1996

Influence of a sympathomimetic amine on masticatory and trapezius pain/pressure thresholds and electromyographic levels.

OBJECTIVES: This study examined the influence of terbutaline, a beta-adrenergic sympathomimetic amine on pain/pressure thresholds in the index fingers and masseter and trapezius muscles and electromyographic activity in trapezii. STUDY DESIGN: In a randomized and double-blind controlled trial, 20 asymptomatic female subjects were assigned to receive either an injection of terbutaline or sterile water before collection of pain/pressure thresholds and electromyographic levels. Repeated analysis of variance and paired t tests were calculated to test for baseline and postinjection differences between groups. RESULTS: No significant baseline or postinjection group differences in pain/pressure thresholds or electromyographic were detected. CONCLUSIONS: beta-adrenergic sympathomimetic stimulation does not influence pain/pressure thresholds or electromyographic activity in the masselet and trapezius muscles or pain/pressure thresholds in the index fingers. These results suggest that development of painful muscle conditions is not caused by elevations of sympathetic activity.

Adolescent↗