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PubMedDate not supplied

Comparison of the myotonolytic activity of tizanidine, eperisone and afloqualone in mouse and rabbit.

The central muscle relaxant activity of the antispastic agent tizanidine was compared with that of two novel clinical agents, afloqualone and eperisone, in the mouse and rabbit. Oral tizanidine strongly inhibited morphine-elicited Straub tail induction in the mouse, showing a median effective dose (ED50) of 1.2 mg/kg. Intravenous tizanidine also inhibited hind limb extensor reflex activity in the rabbit with an ED50 of 0.02 mg/kg. Afloqualone and eperisone, however, were much weaker in the mouse assay with ED50 values of 8.2 and 58.1 mg/kg, respectively. At respective intravenous doses of 2.0 and 1.0 mg/kg, afloqualone and eperisone caused maximally 32% and 41% inhibition of reflex activity in the rabbit. On this basis, afloqualone might be expected to exhibit moderate myotonolytic activity in rheumatological indications, but to be of questionable value in spasticity. Similarly, clinical myotonolytic activity of eperisone would only be expected at high doses unless its functional bioavailability were to be much better in man than in either the mouse or rabbit.

Animals↗
PubMed1986

Bupropion effects in attention deficit and conduct disorders.

Children with Attention Deficit and/or Conduct Disorders were treated with bupropion, a new antidepressant, to determine its clinical, cognitive, and EEG effects. Seventeen male patients (age range 7 to 13.4 years; mean 10.4) participated in an open clinical trial consisting of a baseline placebo period (4 weeks), bupropion therapy (8 weeks), and post-drug placebo (2 weeks). Evaluations included clinical assessments, parents, teachers, and self-ratings; cognitive tests and blood level measurements of bupropion. Fifteen patients received a daily maximum of 150 mg, one received 100 mg and one 50 mg. Clinical global improvement with bupropion therapy was marked in 5 patients, moderate in 7, mild in 2, and none in 3. The Children's Psychiatric Rating Scale indicated improvements of hyperactivity, withdrawal, anxiety, hostility/uncooperativeness, sleep disorder, antisocial behaviour, neuroticism, depression and eating disturbance. Parents' Questionnaires indicated significant improvements of conduct disorder, anxiety, hyperactivity, muscle tension and psychosomaticism. While no single cognitive test showed significant improvement, all nine tests changed in the positive direction. Adverse effects were infrequent, transient and mild. There were no clinically significant changes of the laboratory values and vital signs. Two weeks following bupropion discontinuation, clinical global improvement was maintained in 8 patients, 7 showed relapses, while 2 remained unimproved. Analyses of computerized EEG revealed that degree of clinical improvement was indexed by baseline EEG parameters and that there were significant bupropion effects on EEG measures. Double-blind trials of bupropion are recommended in child psychiatry disorders.

Adolescent↗
PubMed1986

Kinetics of methaemoglobin production. (1). Kinetics of methaemoglobinaemia induced by the cyanide antidotes, p-aminopropiophenone, p-hydroxyaminopropiophenone or p-dimethylaminophenol after intravenous administration.

Methaemoglobin profiles have been studied by using ISIS, a simulation package, and NONLIN, a non-linear least-squares analysis regression program. A simple kinetic model which satisfactorily describes methaemoglobin profiles after p-aminopropiophenone (PAPP) administration and 4-dimethylaminophenol (DMAP) administration has been developed. The two compounds differed mainly in their effective rates of elimination. The model less satisfactorily described methaemoglobin profiles after p-hydroxyaminopropiophenone (PHAPP) administration.

Aminophenols↗
PubMed1986

Kinetics of methaemoglobin production. (2). Kinetics of the cyanide antidote p-aminopropiophenone during oral administration.

The kinetics of methaemoglobin production by orally administered p-aminopropiophenone (PAPP) was studied by using a kinetic model previously developed to describe methaemoglobinaemia consequent on intravenous injection of PAPP. Both ISIS, a simulation package, and NONLIN, a non-linear least-squares regression analysis program, were used to analyse the data. Some modification of the model was necessary to describe oral profiles and 40-50% of the administered PAPP appeared to be being metabolized at first pass to a non-active metabolite.

Administration, Oral↗
PubMed1987

Effect on blood and plasma cyanide levels and on methaemoglobin levels of cyanide administered with and without previous protection using PAPP.

Hydrogen cyanide was administered intravenously at doses of 0.67 or 1.34 mg kg-1 to beagle bitches after protection with oral p-aminopropiophenone (0.5 mg kg-1). Hydrogen cyanide was also administered to unprotected bitches at the lower level (0.67 mg kg-1) only. PAPP protection caused sequestration of cyanide inside the red cells. In the case of the lower dose of cyanide this resulted in a lower plasma cyanide in protected than unprotected bitches. In the case of the higher dose it resulted in survival, despite 1.34 mg kg-1 being a known lethal dose. It is concluded that prior administration of PAPP ameliorated the effects of cyanide poisoning.

Animals↗
PubMed1991

The formation of methaemoglobin by 4-aminopropiophenone (PAPP) and 4-(N-hydroxy) aminopropiophenone.

Oral dosing of rats with the cyanide antidote 4-aminopropiophenone (PAPP), brought about peak methaemoglobin levels at 15-40 min, but peak levels were attained at at 15-25 min after intravenous dosing. After both oral and intravenous administration at equimolar doses, 4-(N-hydroxy)aminopropiophenone (PHAPP), the putative methaemoglobin-producing metabolite of PAPP, produced higher peak levels of methaemoglobin than PAPP. Plasma from rats injected with PAPP was capable of forming methaemoglobin when added to naive rat erythrocytes. The identity of the metabolite responsible is discussed.

Administration, Oral↗
PubMed1984

Bupropion hydrochloride.

Bupropion is a trimethylated monocyclic phenylaminoketone that is an effective antidepressant in humans. It neither is sedating, anticholinergic, nor cardiotoxic. Its mechanism of action may be related to dopamine, but remains uncertain at this time. Clinical trials comparing bupropion 300-750 mg/d with placebo show it to be superior to placebo in efficacy and as well tolerated. Bupropion, in controlled clinical trials, is as effective as amitriptyline or imipramine, with fewer side effects. The only clinically significant adverse reaction to bupropion in more than 1000 patients studied has been seizure induction at a frequency comparable with that of imipramine. Bupropion appears to be safe and effective in both adult and geriatric depressed patients. Although it appears to be safer and equally efficacious when compared with currently used antidepressants, it has not been tested by routine clinical use.

Animals↗
PubMed1981

Echocardiographic evaluation of acute administration of oxyfedrine in patients with coronary artery disease.

In order to assess the effects of oxyfedrine in ischaemic heart disease, echocardiographic evaluation of left ventricular function was performed 2,5,10,15 and 20 minutes after the intravenous administration of 12 mg oxyfedrine in 15 patients with coronary artery disease without angiographic abnormalities of left ventricular wall motion. The following parameters were measured: heart rate, mean arterial blood pressure, internal dimension in diastole (LVIDd) and in systole (LVIDs) of the left ventricule and the percentage shortening of the LVID (%LVID). There was a significant increase in %LVID (peak 10 minutes after drug administration; p less than 0.001) indicating improved left ventricular function, associated with slight changes in pre-load (LVIDd) and in heart rate, and no variation in mean blood pressure. No abnormalities of contraction were observed after the administration of oxyfedrine. These results suggest that oxyfedrine exerts a direct positive inotropic effect of the myocardium in patients with significant coronary artery stenoses.

Aged↗
PubMed1988

Haemodynamic effects of intravenous and oral alifedrine in patients with cardiac failure.

A randomized, double-blind, double-crossover, placebo-controlled haemodynamic study was undertaken in patients with Grade II/III (NYHA) cardiac failure to examine the acute effects of intravenous alifedrine, 20 mg and 40 mg (17 patients), and oral 40 mg alifedrine (8 of these patients). Patients received single doses of alifedrine and placebo on separate days, with invasive monitoring. Alifedrine resulted in a significant (p less than 0.001), dose-dependent increase in cardiac output. The peak effect (+23% with 20 mg i.v., +42% with 40 mg i.v. and +29% with 40 mg orally) was seen approximately 1 hour after intravenous administration (with about half of these increases still apparent at 3 hours) but developed progressively over 3 hours after oral administration. There were significant reductions (p less than 0.001) in peripheral resistance (peak mean changes -21% with 20 mg i.v., -31% with 40 mg i.v. and -23% with 40 mg orally), but little (less than +/- 6%) observed change in arterial pressure. With intravenous alifedrine, there were significant increases in stroke volume (+19% with 20 mg, +35% with 40 mg, p less than 0.001) with little (5%) change in heart rate (+3% and +7%, respectively, N.S.). With the 40 mg oral dose, there was a small increase in heart rate (+12%, p less than 0.005) associated with a 19% (N.S.) increase in stroke volume. Peak haemodynamic responses to 40 mg alifedrine orally were 50% to 75% of those seen after administration of the same dose intravenously. When assessed 3 hours after administration, responses to the two routes of administration were similar. There were no clinically or statistically significant changes in arterial (non-invasive), pulmonary artery, pulmonary capillary or right atrial pressures with any dose of alifedrine. No significant arrhythmias were noted clinically with the doses studied. Alifedrine, therefore, is an interesting agent, available both orally and intravenously, which is well tolerated and appears to produce marked acute increases in cardiac output with little change in heart rate or blood pressure. Further studies should determine whether these effects are maintained during longer-term therapy and clarify the relative contributions of positive inotropic and peripheral vasodilator activity to the effects observed.

Administration, Oral↗
PubMed1987

Control of prolactin release induced by suckling.

In the present study, the role of dopamine and TRH in suckling-induced PRL release was investigated. Bupropion, a dopamine reuptake blocker, increased hypophysial stalk dopamine levels and inhibited suckling-induced PRL release. A short period of suckling, thought to induce a transient decrease in hypothalamic dopamine release, led to higher PRL levels following an iv injection of TRH than in rats which had not nursed their young for a short period after 4- to 6-h separation. These results, in combination with previous data, suggest that a decrease in hypothalamic dopamine release is important for suckling-induced PRL release. Increased PRL release may be in part due to an augmented hypothalamic release of TRH. Since serotonergic mechanisms seem involved in TRH release, lactating rats were treated with drugs acting on serotonergic pathways. Parachlorophenylalanine and pizotifen did not alter suckling-induced PRL release. Methysergide, a serotonin receptor blocker, prevented this PRL release when administered ip but not when injected into the lateral brain ventricle. Since methysergide is converted peripherally into metabolite(s) with dopamine agonistic activity, its effect on suckling-induced PRL release may be due to this action, rather than to its action on serotonin receptors. Thus, these data do not indicate that serotonergic mechanisms are important for suckling-induced PRL release. Passive immunization against TRH inhibited suckling-induced PRL release, indicating that TRH is a hypophysiotropic mediator of this PRL release.

Animals↗