Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “SYMPATHOMIMETICS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 217 records · Page 12Linked to original sources
PubMed1987

Role of cardioselectivity and intrinsic sympathomimetic activity in beta-blocking drugs in cardiovascular disease.

The significance of ancillary properties of beta blockers continues to be the focus of considerable clinical investigation. Beta 1-selective blocking agents, such as acebutolol, inhibit cardiac beta 1 receptors, but have less influence on bronchial and vascular beta 2 receptors. Certain beta 1-selective blocking drugs, including acebutolol, have intrinsic sympathomimetic activity (ISA), also termed partial agonist activity. This property produces slight cardiac stimulation, which can be blocked by propranolol. Drugs with mild or moderate ISA have proven to be as clinically effective as beta blockers lacking this property. Additionally, drugs with ISA possess potential therapeutic benefits, particularly for patients with coronary artery disease. The hemodynamic influences of cardioselectivity and ISA on left ventricular function, heart rate, cardiac output, left-sided heart filling pressure and myocardial oxygen consumption in patients with coronary artery disease are now clearly defined.

Adrenergic beta-Antagonists↗
PubMed1987

Clinical significance of beta 1-selectivity and intrinsic sympathomimetic activity in a beta-adrenergic blocking drug.

Almost all beta-adrenergic blockers, regardless of their pharmacologic characteristics, appear to have blood pressure-lowering activity in hypertensive patients. Comparisons between nonselective beta-blocking agents, such as propranolol and nadolol, with beta 1-selective drugs, such as metoprolol, atenolol and acebutolol, have demonstrated close similarities in their antihypertensive effects in patients. Similarly, beta blockers with and without intrinsic sympathomimetic activity (ISA) have comparable antihypertensive effects. However, beta-selective agents may offer some advantages over conventional beta blockers in hypertensive patients with concurrent conditions such as chronic obstructive airways disease, peripheral vascular disease, diabetes and hyperlipidemia. Beta 1-selective drugs are also preferred in diabetic patients receiving hypoglycemic agents because they do not interfere with glycogenolysis. Agents lacking ISA, such as propranolol, acutely increase peripheral resistance. beta blockers with ISA usually lower resistance. ISA may also minimize the bradycardia frequently found in elderly patients. Agents with ISA may protect against the decrease in high density lipoprotein cholesterol and the modest increase in triglycerides noted with some beta blockers that do not have ISA. Thus, in a large number of clinical situations in which hypertension is found, the properties of beta 1 selectivity and ISA allow beta blockers to be used with greater safety. Therefore, agents possessing both of these properties may be particularly valuable.

Adrenergic beta-Agonists↗
PubMed1987

Impact of beta 1 selectivity and intrinsic sympathomimetic activity on potential unwanted noncardiovascular effects of beta blockers.

Beta-adrenoceptor-blocking drugs are widely used as effective antihypertensive and antianginal agents, but treatment with these agents may be contraindicated in hypertensive patients in whom receptor blockade would interfere with noncardiovascular activities dependent on sympathetic drive. beta blockade impairs pulmonary function in asthmatic patients through antagonism of beta 2 bronchodilation. However, patients with chest problems may be treated effectively with beta 1-selective drugs, including acebutolol, atenolol and metoprolol. The metabolic response to hypoglycemia, which is mediated by beta-receptor stimulation, involves insulin release, gluconeogenesis, tachycardia and increased systolic pressure. Beta 1-selective drugs are preferred in patients who need to increase blood glucose levels because they do not interfere with glycogenolysis. Hypertension induced by pregnancy may be treated with a beta blocker with no apparent adverse effects on the fetus or neonate. Those possessing intrinsic sympathomimetic activity may be preferable.

Adrenergic beta-Antagonists↗
PubMed1987

Treatment of acute intrapartum fetal distress by beta 2-sympathomimetics.

Patients with a diagnosis of severe intrapartum fetal distress by fetal heart rate and capillary blood pH monitoring received beta 2-sympathomimetics to inhibit uterine contractions (tocolysis) while the obstetric team was preparing to deliver the fetus. Fetal heart rate and acidosis significantly improved after tocolysis; these fetuses were subsequently delivered in very good metabolic and clinical condition. The favorable effect of tocolysis on fetal homeostasis is attributed to the suppression of the ischemic effect of contractions on the placental circulation. The few fetuses having an extremely compromised placental function showed no improvement in heart rate or acidosis with tocolysis and were immediately delivered. Considering the mild side effects observed, the lack of maternal complications, and the remarkable perinatal outcome obtained, we recommend using tocolysis before delivering distressed fetuses.

Female↗
PubMed1977

Effect of sympathomimetic amines on the synaptosomal transport of noradrenaline, dopamine and 5-hydroxytryptamine.

The interaction of sympathomimetic amines with the transport of 3H-noradrenaline (3H-NE), 3H-dopamine (3H-DA) and 3H-5-hydroxytryptamine (3H-5-HT) were investigated in rat hypothalamic (3H-NE) and striatal (3H-DA) and 3 H-5-HT) synaptosomes. Modifications in the phenylethylamine structure led to changes in activity towards biogenic amine uptake and release: (a) the introduction of a beta-OH group led to compounds less active in inhibiting uptake and stimulating release of 3H-NE, 3H-DA and 3H-5-HT, with the exception of 3H-NE release which was stimulated more by unlabeled 1-NE than by DA; (b) the introduction of phenolic-OH groups always led to compounds which were stronger uptake inhibitors and releasers of the three biogenic amines; (c) the alpha-methylation increased the potency towards uptake inhibition and release stimulation, with the exception of 3H-NE release: in fact, the releasing activity of phenylethylamine was suppressed by alpha-methylation; (d) the introduction of a -Cl group in the para position selectively potentiated the effects on 3H-5-HT uptake and release and generally depressed those on catecholamine transport.

Animals↗
PubMed1978

Inhibition of synaptosomal uptake of norepinephrine and dopamine by conformationally restricted sympathomimetic amines.

The conformationally restricted cis and trans isomer of substituted cyclobutanes were examined for their ability to inhibit 3H-norepinephrine and 3H-dopamine accumulation by synaptosomes prepared from the cortex and corpus striatum, respectively. The drugs were more effective in preventing the accumulation of 3H-norepinephrine by cortical synaptosomes than 3H-dopamine by striatal synaptosomes. However, in the synaptosomes isolated from both regions, the trans isomers were more potent inhibitors of accumulation than the cis isomers. The greatest stereoselectivity was exhibited by the isomers of 2-amino-1-phenylcyclobutanol. The accumulation of 3H-norepinephrine by cortical synaptosomes and the accumulation of 3H-dopamine by striatal synaptosomes were inhibited 50% by concentrations of the trans isomer of 7.4 X 10(-6) M and 1.7 X 10(-4) M, respectively. The cis isomer was inactive. In separate experiments, the releasing capabilities of the restricted analogs were determined by superfusing cortical and striatal synaptosomes labelled in vitro with 3H-catecholamines. The trans and cis isomers elicited a trivial release of 3H-norepinephrine and 3H-dopamine from cortical and striatal synaptosomes, respectively. The results indicate that the decreased synaptosomal accumulation of 3H-catecholamines caused by the analogs was due mainly to inhibition of uptake. The influence of dihydral angle between phenyl--NH2 on the inhibition of uptake is discussed. It is concluded that the anti conformation of sympathomimetic amines is the preferred conformation at the noradrenergic amine pump.

Aminophenols↗
PubMed1980

The effect of sympathomimetic agents on noradrenaline efflux from a blood vessel.

The effect of several sympathomimetic agents on the efflux of noradrenaline and its metabolites has been evaluated using the ventral artery of the rat tail as the experimental model. This vessel is richly endowed with sympathetic nerves and is therefore well suited to examine the efflux patterns of that transmitter. Etilefrine, tyramine, ephedrine and REN-293 were all found to increase the efflux of 3H-noradrenaline and/or 3H-DOPEG to different degrees from the artery. Possible reasons for this variation in metabolite efflux are discussed.

Animals↗
PubMed1987

Hypokalemic periodic paralysis with unusual responses to acetazolamide and sympathomimetics.

Five members in three generations of a family were affected by an illness that had many clinical features of the hypokalemic form of periodic paralysis (HPP). The serum potassium was either moderately reduced or normal during attacks, and there was no evidence of myotonia or cold-intolerance. All of the patients improved to a variable degree with oral potassium supplements, and 3 responded favorably to triamterene. The usually beneficial drug acetazolamide, however, invariably caused weakness in these patients, an effect previously described in only one other family with HPP. In addition, amphetamine-like sympathomimetic drugs effectively aborted or prevented paralysis in several members. Muscle biopsy in two patients revealed some unusual features, and electromyography showed myopathic potentials. There was no evidence of diabetes. The urine electrolyte concentrations during glucose tolerance tests, however, were different from those previously reported in HPP. This family may represent a variant form of HPP.

Acetazolamide↗
PubMed1984

Genetically obese C57BL/6 ob/ob mice respond normally to sympathomimetic compounds.

The suggestion that defective thermoregulatory thermogenesis in the genetically obese (ob/ob) mouse is due to a low thermic response to noradrenaline has been investigated using both noradrenaline and the longer-acting sympathomimetic compounds, ephedrine and BRL 26830A. Below thermoneutrality (23.5 degrees C) the metabolic rate of obese mice was lower than that of their lean littermates, whereas at a thermoneutral temperature (31 degrees C) the metabolic rate of the obese mice was as high as that of lean mice. This confirms the view that the ob/ob mouse has defective thermoregulatory thermogenesis. However, in C57BL/6 mice, this defect is not due to a failure to respond to noradrenaline, because at 31 degrees C the maximum thermic effects of noradrenaline, ephedrine and BRL 26830A were as high in obese as in lean mice and at 23.5 degrees C they were higher in obese than in lean mice. Furthermore, the response of brown adipose tissue to beta-adrenoceptor stimulation appears normal since noradrenaline caused a normal rise in brown adipose tissue temperature, and treatment with noradrenaline or BRL 26830A in vivo caused a normal increase in GDP binding by brown adipose tissue mitochondria. At 31 degrees C propranolol depressed metabolic rate equally in lean and obese C57BL/6 mice, whereas at 23.5 degrees C it depressed metabolic rate more in lean than obese mice. In contrast to C57BL/6 mice, Aston ob/ob mice showed a reduced thermic response to noradrenaline. These results suggest that defective thermoregulatory thermogenesis in the ob/ob mouse is primarily due to a reduced ability to raise sympathetic tone, but in some strains an additional failure in the thermic response to noradrenaline may develop.

Adipose Tissue, Brown↗
PubMedDate not supplied

Evidence that mCPP-induced anxiety in the plus-maze is mediated by postsynaptic 5-HT2C receptors but not by sympathomimetic effects.

1-(3-Chlorophenyl)piperazine (mCPP) (0.125-1.0 mg/kg i.p.), previously shown to inhibit social interaction, dose-dependently reduced exploration of the open arms of an elevated plus-maze. These findings suggest anxiogenic properties. The effect of mCPP was more potently inhibited by 1-(1-naphthyl)piperazine than by ketanserin, indicative of its mediation via activation of 5-HT2C rather than 5-HT2A receptors. The 5-HT1B receptor agonist CGS 12066B did not antagonise the anxiety-like response to mCPP, and further reduced exploration at the highest dose tested (10 mg/kg i.p.). Depletion of serotonin (5-HT) by p-chlorophenylalanine (PCPA, 150 mg/kg/day x 3) did not prevent the response, although PCPA itself increased open arm exploration. The 5-HT1A/B and beta-adrenoceptor antagonist 1-propanolol (5 mg/kg i.p.) and the peripheral beta 1-receptor antagonist atenolol (20 mg/kg i.p.) showed no significant activity on the plus-maze either alone or against the anxiogenic effect of mCPP. These results indicate that mCPP induces anxiety in the rat in the elevated plus-maze primarily by stimulation of postsynaptic 5-HT2C receptors, and suggest that sympathomimetic effects of mCPP are not involved.

Adrenergic beta-Antagonists↗
PubMed1979

Similar effects of a monoamine oxidase inhibitor and a sympathomimetic amine on memory formation.

Amnesia resulting from inhibition of cerebral protein synthesis by cycloheximide can be prevented by subcutaneous injection of the monoamine oxidase inhibitor pargyline (25 mg/kg) or the sympathomimetic amine metaraminol (3.0 mg/kg) administered up to 30 min following learning of a single trial passive avoidance task in day-old chickens. The injection has to be made during the life time of labile memory for the prevention of cycloheximide-induced amnesia. On the other hand, amnesia induced by the Na/K ATP'ase inhibitor ouabain can only be prevented if these two agents are administered up to 5 min after learning, i.e. during the life time of short-term memory. In addition, both agents produce a retrieval deficit 90 min after the injection, but only when memory is in long-term storage. These results are compared to those obtained with administration of norepinephrine, d-amphetamine and diphenylhydantoin.

Animals↗
PubMedDate not supplied

The selective induction of cellular damage within neoplasia in situ; a putative role for sympathomimetic agents.

Cancerous cells can be selectively injured within a host by various means. The effects generally appear to be manifested indirectly, and are consistent with the concept that uptake from the plasma of non-esterified fatty acids (NEFAs) by malignant tissue leads to an increase in uncoupling of oxidative phosphorylation. Certain lipolytic agents are already known to cause selective damage to cancerous growths in situ. The employment of appropriate sympathomimetic agents to accentuate the nocturnal rise in plasma NEFA concentrations may permit the management and control of a variety of human neoplasia.

Fatty Acids, Nonesterified↗
PubMedDate not supplied

The identification of sympathomimetic amines by Raman spectroscopy.

This study was undertaken to explore the feasibility of using Raman spectroscopy as a means of identifying drugs in the forensic laboratory. Raman spectra of a group of sympathomimetic amines, in pure form and in pharmaceutical preparations, were obtained and compared; group similarities and individual differences were found, and satisfactory identifications could be made. Water solutions as well as solids were examined. The procedure is rapid, sensitive, simple, and non-destructive.

Indicators and Reagents↗
PubMed2004

Chemo- and stereoselective synthesis of benzocycloheptene and 1-benzoxepin derivatives as alpha-sympathomimetic and anorexigenic agents.

The synthesis and pharmacological evaluation of cis- and trans-6-amino-6,7,8,9-tetrahydro-5H-benzocyclohepten-5-ols 4a-c and 5a-c and cis- and trans-4-amino-2,3,4,5-tetrahydro-1-benzoxepin-5-ols 4d-f and 5d-f were carried out. Chemo- and stereoselective synthesis of 5a-f was achieved by reduction of corresponding alpha-amino ketones 3a-f with LiAl(t-BuO)3H. cis-4-Amino-2,3,4,5-tetrahydro-1-benzoxepin-5-ol 4d and trans-4-amino-2,3,4,5-tetrahydro-1-benzoxepin-5-ol 5d exhibited marked anorexigenic activity in mice at a dose of LD50 800 and 500 mg/kg and ED50 75 and 55 mg/kg, respectively, while the analog cis-2,3-dihydroxy-6-amino-6,7,8,9-tetrahydro-5H-benzocyclohepten-5-ol 8 showed typical alpha-sympathomimetic activity.

Amphetamines↗
PubMed1995

Alpha sympathomimetic treatment of autonomic insufficiency with orthostatic hypotension.

PURPOSE: In this double-blind study, the authors compared the safety and efficacy of the investigational oral agent midodrine, a specific alpha 1-sympathomimetic agent, with ephedrine, a nonspecific alpha- and beta-adrenergic receptor agonist. Eight patients (4 men and 4 women) with refractory orthostatic hypotension resulting from autonomic failure were studied. This study was based on the notion that neurogenic orthostatic hypotension results from attenuation of adrenergic nerve traffic and not from alpha-adrenergic receptor dysfunction. Although arteriolar vasoconstrictors seem to be appropriate therapeutic agents, their success has been limited, and the search for an ideal drug is ongoing. METHODS: The authors employed a blocked, double-blind, randomized crossover design. The single-blind placebo run-in period was 2 days. The double-blind titration period with either midodrine or ephedrine was 3 to 5 days; the titration end point was to increase standing systolic blood pressure to > or = 80 mm Hg and to maintain a supine pressure below 180/100 mm Hg. The maintenance period was 3 to 5 days. A 4-day placebo washout period was interposed at the crossover point. RESULTS: The ability to stand improved in patients treated with midodrine but not with ephedrine. Midodrine significantly increased both systolic (P < 0.001) and diastolic (P < 0.001) standing blood pressure over placebo (P < 0.001) and ephedrine (P < 0.05). In contrast, ephedrine-induced changes in standing pressures did not significantly differ from placebo (P > 0.05). Midodrine treatment improved the frequency of the ability to stand as compared with ephedrine, and was associated with a significantly higher incidence of standing systolic pressures > 80 mm Hg than was placebo (P < 0.001). Both midodrine and ephedrine significantly increased supine systolic and diastolic blood pressures over placebo (P < 0.001, P < 0.01, P < 0.01, P < 0.01, respectively), but were not significantly different from each other. Ephedrine significantly increased (P < 0.05) the pulse rate as compared with placebo and midodrine, whereas midodrine produced a statistically significant (P < 0.05) but clinically minimal decrease in pulse rate compared with placebo. Neither drug affected clinical laboratory variables. CONCLUSIONS: Midodrine safely and effectively improved orthostatic hypotension caused by autonomic failure. Our data suggest that the ability to stand is improved better by midodrine than by ephedrine.

Adrenergic alpha-Agonists↗
PubMed1977

Detection of sympathomimetic central nervous stimulants with special reference to doping. II. Comparative study of two adsorption chromatography methods using different XAD resins.

Recoveries of a series of sympathomimetic central nervous stimulants in human urine are measured using either adsorption chromatography on self-filled columns (method A) or with a special resin method suitable for racehorse urine (method B). The Amberlite resins used are XAD-2, XAD-4, XAD-7 and XAD-8 and elution is performed using chloroform. The reported comparative drug extractabilities indicate that in most instances the recoveries follow the sequence XAD-4 greater than XAD-2 approximately XAD-8 greater than XAD-7 using method A. Based on the recovery and purity of the extracts obtained, XAD-8 is preferred for gas chromatographic analysis while XAD-4 is very suitable for thin-layer chromatographic screening work. Comparing the two methods, equally good or better results were obtained with method A for all of the resins studied except XAD-7. Finally, it was found that the effect of refrigerated storage of the resins on the drug extractabilities for central nervous stimulants could be neglected.

Adsorption↗
PubMed1991

[Specific detection of urinary sympathomimetic amines for control of anti-doping by gas chromatography-mass spectroscopy].

A specific, sensitive and reliable gas chromatography-mass spectrometry (GC-MS) technique for detection of sympathomimetic amines following urinary extraction is proposed. Amphetamine, phentermine, ephedrine, mephenorex, methylphenidate, benzphetamine, clobenzorex and internal standard (fenfluramine) are extracted from urines at pH 7.0 using elution by chloroform-isopropanol on C18 cartridges. Derivatization followed by GC-MS analysis allows identification of these drugs founded on relative retention times and mass spectra. The quantitation limit for derivatizable drugs was found to be 200 ng/ml and 500 ng/ml for underivatizable drugs.

Amphetamines↗
PubMed1997

Reversible segmental left-ventricular dysfunction caused by accidental administration of sympathomimetic drug in human.

A inadvertently administrated high dose of sympathomimetic drug induced cardiogenic shock manifestations in a previously healthy woman. This state was characterized by EKG subendocardial injury, serum cardiac enzymes elevation, extensive regional left ventricular wall motion abnormalities on echocardiogram. Therapeutics included oxygen, systemic vasodilators and diuretics. Clinical recovery occurred over a four days period and parallels the normalization of echocardiogram and EKG alterations.

Adult↗