Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1323099 (sympathomimetic)
 2,957 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 18 patients with documented ischaemic heart disease the cardiovascular effects of ketamine (1.5 mg/kg iv) were studied under three different conditions: 1. in awake premedicated patients (n = 6); 2. after the previous administration of flunitrazepam (0.015 mg/kg iv, n = 6) and 3. under conditions of neuroleptanalgesia and muscle relaxation (n = 6). Flunitrazepam prevented or at least attenuated the increases in heart rate (30%), mean arterial pressure (37%), mean pulmonary artery pressure (165%), left ventricular filling pressure (230%), total peripheral resistance (50%), pulmonary vascular resistance (100%) and in the rate-pressure product (66%) which were associated with the use of ketamine as the sole anaesthetic agent. In addition, the flunitrazepam-pretreatment abolished the fall in cardiac index and stroke index which occured in patients given ketamine alone. Flunitrazepam therefore appears to be a promising drug to prevent adverse cardiovascular reactions, when ketamine should be chosen for induction of anaesthesia. Neuroleptanalgesia and muscle relaxation also proved effective in controlling the sympathomimetic actions of ketamine. The response of the mean pulmonary artery pressure and of the ventricular filling pressures to ketamine in this group was even more damped than in the patients pretreated with flunitrazepam alone.
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PMID:[Flunitrazepam-pretreatment for prevention of adverse cardiovascular effects following ketamine]. 4 95

Six healthy volunteers took part in a randomized, single-blind, crossover study to quantitate the intrinsic sympathomimetic activity (ISA) of penbutolol in comparison with one drug possessing ISA (alprenolol) and with the standard non-ISA drug (propranolol). Single intravenous and one week oral administrations were studied. Complete parasympathetic and sympathetic isolation of the heart was obtained by administration of atropine 0.04 mg/kg body weight i.v. and propranolol 0.4 mg/kg i.v., or corresponding equipotent doses of alprenolol 0.4 mg/kg i.v. and penbutolol i.v. 0.08 mg/kg. In the chronic, oral study propranolol 160 mg b.i.d. was given, or corresponding equipotent doses of alprenolol (400 mg b.i.d.) or penbutolol (40 mg b.i.d.). The test procedure included measurement of heart rate and blood pressure in the supine, sitting and standing positions, and during isometric and dynamic exercise. ISA was calculated by comparison of the change in of heart rate with that produced by propranolol. The ISA of alprenolol was 22--26% and of penbutolol 12--18% of maximal sympathetic activity. Isometric and dynamic exercise gave comparable ISA values.
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PMID:Intrinsic sympathomimetic activity of penbutolol. 4 55

The effects of acebutolol, a cardioselective beta-adrenoceptor blocking agent, on the systolic blood pressure and heart rate were investigated in conscious Kyoto Wistar normotensive rats (WKY), spontaneously hypertensive rats (SHR) and DOCA-NaCl hypertensive rats (DOCA rats) and the results compared with those of propranolol and practolol. In WKY and DOCA rats, the intraperitoneal administration of acebutolol, propranolol and practolol (0.5 approximately 20 mg/kg) produced a hypotensive action, however, these effects were observed only with restricted doses and there was no evidence of a dose-dependency. The heart rate was decreased by acebutolol and propranolol, but was increased by practolol which possesses an intrinsic sympathomimetic activity. In SHR, propranolol produced a dual action, a slight rise followed by a slight fall, the change not being significant, while practolol induced a slight hypertension. On the other hand, acebutolol in high doses induced a dose-dependent hypotensive action. The heart rate was markedly and dose-dependently decreased by these three agents. Thus, while propranolol and practolol produced hypotensive effects in WKY and DOCA rats, acebutolol produced hypotensive effects in WKY, SHR and DOCA rats. These results suggest that acebutolol is a beta-adrenoceptor blocking agent which possesses hypotensive activity in hypertensive rats.
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PMID:[Effect of acebutolol, a cardioselective beta-adrenoceptor blocking agent, on the blood pressure in rats (author's transl)]. 4 60

The suggested use of etilefrine in the treatment of patients with orthostatic hypotension is based on the premise that it has an action similar to that of noradrenaline (Miller, Wiener and Bloomfield, 1973). However, earlier work from this laboratory (Frost, Frewin and Gerke, 1977; Frost, Frewin, Gerke and Downey, 1978; Frost, Halloran, Frewin, Gerke and Downey, 1978) on blood vessels in the rat tail has suggested that the drug acts predominantly as an indirect sympathomimetic agent. The present study examined the action of etilefrine on the central artery of the rabbit ear. This vessel is known to have a rich sympathetic innervation (de la Lande, Frewin and Waterson, 1967) and has the added advantage that it can be surgically denervated. It therefore became possible to examine the effects of etilefrine on both normal and denervated arteries and to quantitate the extent to which the drug relied on the symphathetic nerves for its vasoconstrictor effects.
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PMID:Vascular effects of etilefrine. Further studies to substantiate the predominant indirect sympathomimetic action of this agent. 4 69

1 Bronchodilator efficacy of four beta 2-sympathomimetic aerosols, fenoterol, orciprenaline, salbutamol and terbutaline has been compared in nine patients with chronic stable reversible airways obstruction using a double-blind placebo controlled cross-over design. Two puffs of each agent were given on two separate occasions to each of the patients and the forced expiratory volume in one second (FEV1) and the vital capacity (VC) were measured before and 30, 90, 150 and 210 min after administration. 2 Multivariate analysis of the data at 30 min showed FEV1 and VC in these patients to be so highly correlated that they could be considered as a single variable. 3 When absolute change in VC at 30 min was used as the response criterion, efficacy of the four drugs was significantly better than placebo (P < 0.01). It was not possible to rank all four drugs in order of effectiveness; fenoterol and salbutamol were significantly better than terbutaline and orciprenaline (P < 0.01) but this was complicated by a significant interaction effect between drugs and patients (P < 0.01). 4 Similar results were obtained when absolute and relative changes in FEV1 and VC and area under the curve were used as response variables. 5 The study demonstrates that important individual differences in patient response may be concealed if only average drug effects are considered.
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PMID:Cross-over study of the efficacy of four beta 2-sympathomimetic bronchodilator aerosols. 4 95

Isolated vas deferens preparations from 16 rabbits of the New Zealand white strain were subjected to electrical and chemical excitability under physiological conditions and under the influence of drugs. Such smooth muscle fibres were strictly confined to the terminal 3 cm. segments of the distal 'urethral' portions of the vasa deferentia. Intermittent field stimulation, at 60 second intervals, was provided by a stimulator of low output impedance under constant parameters of voltage, pulse width and frequency. Results from this investigation revealed the undermentioned anomalous but distinct findings viz: (a) the presence of a minor adrenergic component which disappeared in phentolamine but remained unaffected by prolonged exposures to phenoxybenzamine; (b) the presence of a predominantly non-adrenergic component which was totally refractory to phenoxybenzamine but suffered a weak diminution in phentolamine; and (c) the picture of a phentolamine-insensitive but twitch-inhibiting effect shared by both tyramine and noradrenaline. Rabbit vasa consistently displayed a remarkable insensitivity to the motor effects of submicromolar concentrations of the putative neurotransmitter substance i.e. noradrenaline. The indirect sympathomimetic agent, tyramine failed to elicit any contractions when employed in doses as massive as 290 micrometers. i.e. 5 x 10(-5) g/ml, except in 2 out of 14 trials when a weak phentolamine-susceptible bursts of single contractions were produced. Thus, the adrenoceptors involved in the mediation of the twitch-inhibiting effects, appear not to behave towards conventional adrenoceptor antagonists in the classified manner. It seems appropriate therefore to invoke an unknown neurotransmitter for the non-adrenergic component in this motor transmission.
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PMID:Evidence for a strong non-adrenergic component in the motor transmission to the rabbit vas deferens. 4 26

The beta-blocking activity of propranolol was studied on the positive inotropic effect of norepinephrine, epinephrine, isoproterenol, dopamine and ethylephrine, in the left atrium driven at different rates. Dose of the antagonist of 10(-8) and 10(-7) M did not block the norepinephrine dose-response curve at 1 and 2.8 Hz, but a shift to the right was observed at 1.6 Hz. Although epinephrine showed a significant increase in its pD2 (p less than 0.001) at the lower stimulation frequency, the blockade increased progressively the higher the rates. On the other hand, propranolol antagonized isoproterenol at all the frequencies tested, in spite of an increase in the maxima at 2.8 Hz. This latter behavior was also true for dopamine and ethylephrine. Both sympathomimetic amines were blocked by propranolol at 1 and 1.6 Hz. The complex effect of propranolol on Ca2+ movements and its effects on cAMP and ATPase seem to be superimposed to the beta-blocking activity. Thus, the various actions on the sympathomimetic amines change according to the agonist considered and the stimulation frequency employed.
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PMID:Effect of the frequency of stimulation on the blocker action of propranolol in isolated rat left atria. 4 42

The effect of amantadine-hydrochloride on heart and circulation is studied in 7 anesthetized, otherwise normal dogs with a mean body weight of 27.2 kg and in 8 heart-lung preparations of dogs. Arterial blood pressure, right atrial pressure, cardiac output and heart rate are measured and continuously monitored. Stroke volume and peripheral resistance are calculated. Left ventricular peak- and enddiastolic pressure, the rate of rise of intraventricular pressure and t-dp/dt are additionally measured in the heart-lung-preparations. Below 3 mg with kg(-1) in anesthetized dogs and 10 mg in the heart-lung preparation, respectively, a positive inotropic effect of amantadine is observed. This effect is caused by a liberation of catecholamines. Higher dosage of amantadine decreases cardiac contractility significantly. Therefore the negative inotropic influence of the drug itself has to be distinguished from the indirect sympathomimetic effect resulting from local release of myocardial catecholamines. Cardiac arrhythmias which occur in several experiments, can mostly be eliminated with propranolol or other drugs like lidocaine or sparteinsulphate.
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PMID:[Effects of amantadine on heart and circulation]. 5 42

The model psychosis associated with amphetamine overdosage is known to bear a close resemblance to acute paranoid schizophrenia. Amphetamine is chemically similar to the endogenous sympathomimetic amine, phenylethylamine, which possess many of its pharmacological properties. It is suggested that some cases of schizophrenia may be associated with an abnormal phenylethylamine response, either from increased concentrations of the amine or from abnormal receptor sensitivity to it.
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PMID:Does phenylethylamine cause schizophrenia? 5 86

Study of general haemodynamics in 15 patients with low-renin essential hypertension showed haemodynamic and pathophysiological heterogeneity. However, there was suppression of sympathetic nervous system function in all low-renin patients, regardless of haemodynamic pattern. Subnormal sympathetic nervous activity was manifested by a low normal mean plasma-noradrenaline concentration at rest, diminished noradrenaline responsiveness to postural stimulation, and a reduced blood-pressure response to the indirectly acting sympathomimetic amine tyramine. It is proposed that the syndrome of low-renin essential hypertension is of diverse aetiology, but with secondary sympathetic nervous system underactivity as a feature common to the various forms. The low plasma-renin activity is probably an expression of defective sympathetic nervous system stimulation of renin release.
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PMID:Suppression of sympathetic nervous function in low-renin essential hypertension. 5 83


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