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PubMed1992

Sympathomimetics, inotropics, and vasodilators.

Management of the critically ill patient often necessitates the use of multiple inotropic and vasoactive medications. This article offers a concise, clinical reference to guide the practicing clinician in the use of these agents. The focus is on parenteral agents used for acute rather than chronic management. Physiologic concepts basic to understanding the use of these agents are reviewed briefly. Sympathomimetic agents are discussed with inotropes since many of them have cardiotonic properties. Vasodilator therapy is addressed only as it is used in combination therapy. Nursing implications and treatment regimes are included.

Cardiotonic Agents↗

PubMed1999

Kinetic analysis of drug-receptor interactions of long-acting beta2 sympathomimetics in isolated receptor membranes: evidence against prolonged effects of salmeterol and formoterol on receptor-coupled adenylyl cyclase.

The long-acting beta2 sympathomimetics salmeterol and formoterol have been presumed to exert their prolonged action either by binding to an accessory binding site ("exo-site") near the beta2 adrenoceptor or by their high affinity for beta2 adrenoceptors and correspondingly slow dissociation. Whereas most studies with salmeterol had been done in intact tissues, which have slow diffusion and compartmentation of drugs in lipophilic phases, that restrict drug access to the receptor biophase, we used purified receptor membranes from rat lung and disaggregated calf tracheal myocytes as model systems. Binding experiments were designed to measure the slow dissociation of agonists by means of delayed association of (-)-[125I]iodopindolol. Rat lung membranes were pretreated with high concentrations of agonists (salmeterol, formoterol, isoprenaline) before dissociation was induced by 50-fold dilution. Half-times of association of (-)-[125I]iodopindolol remained unchanged compared with untreated controls, indicating that dissociation of agonists occurred in less than 2 min. Adenylyl cyclase experiments were designed to determine the on and off kinetics of agonists to beta2 adrenoceptors by measuring the rate of receptor-induced cyclic AMP (cAMP) formation. Experiments were performed in tracheal membranes characterized by high Vmax values of cAMP formation. Adenylyl cyclase activation occurred simultaneously with the addition of the agonist, continued linearly with time for 60 min, and ceased immediately after the antagonist was added. Similarly, when receptor membranes were preincubated in a small volume with high salmeterol concentrations, there was a linear increase in cAMP formation, which was immediately interrupted by a 100-fold dilution of the reaction mixture. This militates against the exo-site hypothesis. On the other hand, dissociation by dilution was much less when membranes were preincubated with a large volume of salmeterol at the same concentration, indicating that physicochemical effects, and not exo-site binding, underlie its prolonged mode of action.

Adenylyl Cyclases↗

PubMed1998

[Synchronization of secretion of the evoked transmitter quanta as mechanism of the facilitating action of sympathomimetics].

Noradrenaline, isoproterenol, dobutamine were found to modulate kinetics of quanta secretion so as to synchronize the transmitter release. This effect could be prevented with blocking agents of beta-adrenoreceptor (atenolol, propranolol). Activators of beta-adrenoreceptors klonidine and phenylephrine did not change the kinetics of quanta secretion, whereas phentolamine did not affect the synchronizing effect of noradrenaline. The change in the time course of the secretion induced by noradrenaline increased the end-plate current amplitude. There seems to exist a specific presynaptic mechanism involving beta-adrenoreceptors for facilitation of effects of sympathomimetics.

Action Potentials↗

PubMed1999

The effects of intrinsic sympathomimetic activity on beta-blocker efficacy for treatment of neurocardiogenic syncope.

To compare the efficacy and side effects of beta-blockers with intrinsic sympathomimetic activity (ISA) to those without ISA, we retrospectively reviewed patients diagnosed with neurocardiogenic syncope (NCS) as determined by head-up tilt table testing. Four hundred and thirty-one patients (mean age of 57 +/- 25 years) underwent head-up tilt table testing for syncope of unknown etiology, of which 120 patients were diagnosed with NCS; 87 of these patients were treated with beta-blocker therapy. Only 56 patients could be contacted during follow-up. Twenty-eight patients were treated with beta-blockers with ISA (acebutolol or pindolol) and 28 received beta-blockers without ISA (atenolol or metoprolol) based on physician preference and followed for up to 2 years. During the follow-up period, beta-blockers with or without ISA had comparable clinical efficacy in suppressing recurrent syncope in patients with NCS. However, beta-blockers with ISA were better tolerated and caused less fatigue (32% side effects) as compared to those without ISA (50% side effects; p = 0.23). The benefits of beta-blockers with ISA were more pronounced in patients less than 60 years old (19% side effects with beta-blocker with ISA as compared to 85% side effects with beta-blocker without ISA; p = 0.0004). Beta-blockers without ISA appear to be better tolerated and caused less fatigue in patients 65 years old or greater (20%) than in patients less than 65 years old (85%; p = 0.0002).

Acebutolol↗

PubMed1976

Evaluation of intrinsic sympathomimetic activity of beta-adrenoceptor blocking drugs in the treatment of patients with angina pectoris.

Beta-adrenoceptor blocking drugs with intrinsic sympathomimetic activity (ISA) may be less effective in the treatment of patients with angina pectoris than some others that lack this property. A review of 14 trials comparing beta-adrenoceptor blocking drug with ISA and those without ISA in angina pectoris has been made. The overall picture emerges from both acute and chronic studies using subjective and objective endpoints, that there is no striking difference in effectiveness between the two kinds of beta-adrenoceptor blocking drugs. The one exception is pindolol (a drug with ISA) which, at higher doses, has been shown to be consistently worse than propranolol (a drug without ISA). The reasons for the similarity between propranolol and other bets-blocking drugs with ISA in the trials cited are either that the trial design was defective (the trials were mainly fixed dose comparisons) or that the stimulant effects of those drugs with ISA is not of sufficient magnitude to make a difference. It is suggested that further carefully constructed clinical trials should be carried out before the second reason can be accepted.

Acute Disease↗

PubMedDate not supplied

Determination of phenolic sympathomimetic drugs in pharmaceutical samples and biological fluids by flow-injection chemiluminescence.

A rapid and highly sensitive flow-injection chemiluminometric method was developed for determination of 3 sympathomimetic drugs, namely, etilefrine hydrochloride, isoxsuprine hydrochloride, and prenalterol hydrochloride. The method is based on chemiluminescence induced by oxidation of drugs with acidified potassium permanganate in the presence of formic acid as a carrier. The calibration graphs were linear over the concentration ranges 0.2-9, 0.2-12.5, and 0.025-1.25 microg/mL for the 3 compounds, respectively. The method was applied successfully in determining the drugs in dosage forms and in biological fluids. A proposal for the reaction pathway is suggested.

Calibration↗

PubMed1994

Human cardiovascular response to sympathomimetic agents during head-down bed rest: the effect of dietary sodium.

Changes in sympathoadrenal function and cardiovascular deconditioning have long been recognized as a feature of the physiological adaptation to microgravity. The deconditioning process, coupled with altered hydration status, is thought to significantly contribute to orthostatic intolerance upon return to Earth gravity. The cardiovascular response to stimulation by sympathomimetic agents before, during, and after exposure to simulated microgravity was determined in healthy volunteers equilibrated on normal or high sodium diets in order to further the understanding of the deconditioning process.

Adult↗

PubMedDate not supplied

[Sympathomimetic enantiomers: correlation between configuration and effect on neuronal catecholamine uptake].

A mechanism responsible for the difference in the activity of enantiomers of sympathomimetics (SMs) as inhibitors of the neuronal uptake of catecholamines was studied using the SM molecular models built in preferred conformations at the binding sites. It is shown that the substituents of SM enantiomers interacting with the binding sites of membrane transporters may occupy both energetically favorable and unfavorable (configuration-dependent) positions at the asymmetric carbon atoms. Estimating the positions of these substituents, it is possible to rationalize a relationship between the configuration of SM enantiomers and the rank order of their inhibiting potency.

Binding Sites↗

PubMed1992

Further metabolic studies of codeine and morphine in mice pretreated with sympathomimetics.

The effects of ephedrine and phenylpropanolamine (PPA) on the 24 h urinary excretion of morphine, codeine and their metabolites, and on the plasma and brain disposition of morphine and codeine at steady state in mice were studied. Morphine-3-glucuronide was the major urinary metabolite in morphine treated animals, while for codeine treated animals norcodeine and morphine-3-glucuronide were the major metabolites. In all cases percentage of drug excreted unchanged was 10-15% of the administered dose. Ephedrine or PPA pretreatment had no apparent effect on these parameters. The metabolic ratios for the different pathways were comparable in all treatment groups. Steady-state plasma and brain concentration-time profiles of codeine and morphine also showed marked similarity in all treatment groups. Apparently, ephedrine or PPA pretreatment has no effect on the disposition of morphine and codeine in mice. The results are discussed from the perspective of our earlier findings of dependence on cough mixtures containing opioids and sympathomimetics.

Animals↗

PubMed2006

[Sympathomimetic syndrome caused by autointoxication with methylphenidate].

A 31-year-old man claimed that he had ingested more than 100 tablets of methylphenidate (10 mg), 20 tablets ofibuprofen (400 mg) and 2 bottles of wine. At admission, signs of sympathomimetic syndrome were observed, including agitation, hallucinations, mydriasis and sinus tachycardia. The patient was treated with activated charcoal and an oral laxative. Given the possibly lethal dose of methylphenidate, the patient was admitted to the intensive care unit for observation. He made a full recovery and was discharged 36 hours after admission. Toxicological analysis indicated a plasma-ethanol concentration of 0.27% and a maximum serum-methylphenidate concentration of 176 microg/l (therapeutic range: 5-40 microg/l). The active metabolite ethylphenidate was also present at toxic concentrations. Treatment of potentially lethal methylphenidate poisoning includes prevention of absorption, careful observation and support of vital functions as necessary.

Adult↗

PubMed1991

Effects of sympathomimetic agents on opiate analgesia, tolerance and dependence in mice.

The effects of chronic pretreatment with ephedrine and phenylpropanolamine (PPA) on the antinociceptive activities of morphine and codeine, as well as their effects on the induction and expression of tolerance to, and dependence on morphine and codeine in mice are reported. Chronic pretreatment with ephedrine or PPA attenuated the antinociceptive effects of subsequently administered morphine or codeine. When administered during the induction phase, sympathomimetics enhanced opiate tolerance with little or no effect on the development of physical dependence. Given in the expression phase, ephedrine and PPA did not significantly affect tolerance, whereas there was significant suppression of withdrawal signs. The possible implications of these results are discussed.

Analgesia↗

PubMed1977

Tremor caused by sympathomimetics is mediated by beta2-adrenoreceptors.

Tremor caused by beta-adrenostimulating drugs is known to be mediated by beta-receptors in skeletal muscles. In this study it was shown that tremor caused by terbutaline could be blocked by propranolol, a drug with both beta1- and beta2-blocking properties, but not by metoprolol, a beta1-selective antagonist. It is concluded that tremor caused by sympathomimetics in man is mainly mediated by beta2-receptors.

Blood Pressure↗

PubMedDate not supplied

Liquid chromatographic determination of six sympathomimetic drugs in dosage forms.

A simple and rapid stability-indicating liquid chromatographic method is described for quantitative determination of 6 sympathomimetic drugs in various liquid and solid formulations. Analyses were carried out on a C18 reverse phase column using 0.01M 1-octanesulfonic acid, sodium salt in 0.2% acetic acid-methanol (70 + 30) as the mobile phase with photometric detection at 220 nm. Coefficients of variation for 5 consecutive injections of a mixed standards solution ranged from 0.62% for metaraminol to 1.40% for epinephrine. Standard recoveries ranged from 98.8% for metaraminol to 100.8% for epinephrine. The method was linear between 0.2 and 10 micrograms of drug injected and was used successfully to analyze 17 commercial products in a variety of dosage forms.

Chromatography, Liquid↗

PubMed1990

Sympathomimetics.

Sympathomimetics have a long history of abuse. Initially amphetamines were abused for their adrenergic "rush"; now more sophisticated chemists have developed compounds that add a hallucinogenic component. Since the advent of crack and now "ice," the physician needs to recognize and treat appropriately those patients who present with the signs and symptoms of sympathetic hyperactivity.

Ambulatory Care↗

PubMed1986

Differential changes in lymphocyte beta 2-adrenoceptor density by beta-blocker administration: role of intrinsic sympathomimetic activity.

To study the role of intrinsic sympathomimetic activity (ISA) in beta-blocker-induced changes of beta-adrenoceptors, the effects of administration of several beta-blockers for 9 days on lymphocyte beta 2-adrenoceptor density--assessed by 125iodocyanopindolol binding--were investigated in 47 normotensive volunteers. Propranolol (unselective; no ISA; 4 X 40 mg/day) increased beta 2-adrenoceptor density by 25-40%; after withdrawal beta 2-adrenoceptor density declined slowly, being still elevated for 3 days. In contrast, the unselective beta-blockers pindolol (ISA (isoprenaline = 1.0) = 0.39; 2 X 5 mg/day) and mepindolol (ISA = 0.27; 2 X 5 mg/day) decreased beta 2-adrenoceptor density by 50% and 35%, respectively, while alprenolol with weak ISA (=0.066; 4 X 100 mg/day) had no effect. Among the beta 1-selective blockers studied, celiprolol with ISA (=0.32; 1 X 200 mg/day) decreased beta 2-adrenoceptor density by 30% whereas bisoprolol without ISA (1 X 10 mg/day) had no effect. It is concluded that the ISA determines the direction and amount of beta-adrenoceptor alterations induced by beta-blockers. Furthermore, changes in human lymphocyte beta-adrenoceptors reflect subtype-selective changes in beta 2-adrenoceptors, since the beta 1-selective blocker bisoprolol without ISA--in contrast to propranolol--did not affect lymphocyte beta 2-adrenoceptors. Accordingly, the fact that the beta 1-selective blocker celiprolol with ISA decreased lymphocyte beta 2-adrenoceptors, is consistent with the hypothesis that celiprolol possesses in addition to its beta 1-antagonistic activity a beta 2-agonistic activity.

Adrenergic beta-Antagonists↗

PubMed1976

The significance of beta1-beta2-selectivity and intrinsic sympathomimetic activity in beta-blockers, with particular reference to antihypertensive treatment.

From the findings described in the already fairly copious literature on antihypertensive therapy with beta-blockers, as well as on the basis of theoretical considerations, it may be concluded that neither cardio-selectivity nor intrinsic sympathomimetic activity is of decisive importance with regard to the blood-pressure-lowering action of these these compounds. As far as hypotensive potency alone is concerned, none of the known beta-blocking agents is fundamentally superior to the others. There are, however, considerable differences between them in respect of their safety in use, tolerability and side effects, and during long-term treatment especially these must be taken into account.

Adrenergic beta-Antagonists↗

PubMed1986

Pharmacological studies on the intrinsic sympathomimetic activity of the beta-adrenoceptor antagonist mepindolol.

1-Isopropylamino-3-(2-methyl-4-indolyloxy)-2-propanol (mepindolol, Corindolan) is a beta-adrenoceptor antagonist with significant intrinsic sympathomimetic activity (ISA): positive chronotropic effects in atria of the rat amount to 24% of those elicited by the full agonist isoprenaline. Relaxant effects in blood vessels approach 50% of those of isoprenaline. This vasorelaxant effect is completely blocked by the specific beta 2-adrenoceptor antagonist ICI 118 551 (erythro-dl-1-(7-methylindan-4-yloxy)-3-isopropylaminobut an-2-ol), suggesting that the vasodilatory effects of mepindolol are elicited by stimulation of vascular beta 2-adrenoceptors. In the anaesthetized cat mepindolol acutely lowers arterial blood pressure by reducing total peripheral resistance without exhibiting significant cardiodepressant action, whereas propranolol, lacking ISA, lowers blood pressure by a marked reduction of cardiac output and left ventricular contractility, however, total peripheral resistance is significantly increased.

Adrenergic beta-Antagonists↗

PubMed1988

Remission of mild to moderate hypertension after treatment with carteolol, a beta-adrenoceptor blocker with intrinsic sympathomimetic activity.

Previous studies have indicated that some hypertensive patients, following a period of effective treatment with certain antihypertensive drugs, may experience prolonged normotension after drug withdrawal. We have studied the ability of carteolol, a nonselective beta-adrenoceptor antagonist with intrinsic sympathomimetic activity, to produce such remissions of hypertension. Thirty-four patients whose diastolic blood pressure was controlled at 90 mm Hg or less with carteolol monotherapy (2.5 to 5.0 mg/d for an average of 328 days) were randomized to a nine-month, double-blind, placebo-controlled drug-withdrawal trial. Those patients randomized to continue carteolol therapy had initially responded to carteolol treatment with reduction in blood pressure from 151 +/- 4/99 +/- 2 to 132 +/- 4/80 +/- 2 mm Hg. Those randomized to treatment with placebo had initially responded with blood pressure reductions from 154 +/- 4/97 +/- 2 to 137 +/- 4/81 +/- 2 mm Hg. Changes in mean systolic and diastolic blood pressure (mm Hg +/- SEM) from baseline during carteolol therapy to the final visit at nine months were not different for patients receiving placebo (13 +/- 5/6 +/- 4 mm Hg, recumbent; 11 +/- 6/4 mm Hg, standing) or carteolol (11 +/- 5/7 +/- 3 mm Hg, recumbent; 12 +/- 6/7 +/- 3 mm Hg, standing). The final mean recumbent diastolic blood pressure (86.9 mm Hg) was the same in both groups. Prolonged normotension may follow a period of carteolol treatment, again suggesting the potential importance of periodic withdrawal of antihypertensive medication.

Blood Pressure↗