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At least 577 records · Page 32Linked to original sources
PubMed1983

Pharmacological study of the antitussive and respiratory-analeptic properties of N-(2'-ethylpyrrolidino)diphenylacetamide hydrochloride (F 1459).

The antitussive and respiratory stimulant properties of N-(2'-ethylpyrrolidino)diphenylacetamide hydrochloride (F 1459) in animals are reported. In the mechanical stimulation of the trachea in guinea pigs and after intraperitoneal administration of the product, F 1459 showed a better antitussive action as compared to oxeladin, zipeprol, codeine and clobutinol. Low intraduodenal doses of F 1459 also reduced in cats the cough induced by the electrical stimulation of the superior laryngeal nerve. In anesthetized dogs whose respiratory functions had been depressed by morphine, F 1459 significantly increased the volume inspired per minute, an effect not due to any uncoupling effect on oxidative phosphorylation. F 1459 has local anesthetic and broncholytic properties that may play a role in the mechanism of its antitussive action. Contrarily to codeine, the test compound did not induce a decrease in the intestinal transit.

Anesthetics, Local↗
PubMed1982

[Effects of thymo-analeptics and acceptability of amineptin compared to those of imipramine].

Amineptine and imipramine were compared in a double-blind controlled trial carried out in 52 depressed patients over a period of 30 days, with daily doses of amineptine ranging from 100 to 300 mg or of imipramine ranging from 50 to 150 mg. Global assessment of response to treatment and Hamilton rating scale scores showed no significant difference between amineptine and imipramine. Both drugs were effective as soon as the 7th day of treatment, and their efficacy constantly increased during the 30 days of the observation. The clinical acceptability of amineptine is superior to that of imipramine: in the amineptine group acceptability was considered excellent in 67% of the cases; in the imipramine group acceptability was considered excellent in 48%. 8% of the patients in the imipramine group were withdrawn from the trial because of intolerance.

Adolescent↗
PubMed1980

[Synthesis, absolute configuration and mass spectroscopic fragmentation of the circulation analeptic cafedrine (author's transl)].

The synthesis of [R-(R*,S*)]-7-[2-[(2-hydroxy-1-methyl-2-phenylethyl)amino]-ethyl]-3,7-dihydro-1 ,2-dimethyl-1H-purine-2,6-dione (Cafedrine) and its stereoisomers is reported. By means of 1H- and 13C-nmr spectroscopy the relative configuration of the two asymmetric centres is ascertained and the absolute configuration is discussed. The EI-mass spectrometric fragmentation of cafedrine has been elucidated.

Blood Circulation↗
PubMed1989

Effects of a new analogue of thyrotropin-releasing hormone on pentobarbital-induced sleeping time in rodents.

The effects of a new analogue of TRH, YM-14673 (N-[[(S)-4-oxo-2-azetidinyl]carbonyl]-L-histidyl-L-prolinamide dihydrate) on pentobarbital-sleeping time were observed in comparison with those of TRH in rodents. The YM-14673 was administered intravenously, orally and intramuscularly. In all cases it reduced pentobarbital-sleeping time in rats and/or mice in a dose-dependent manner. The analeptic activity of YM-14673 was about 10 times greater than that of TRH. Analeptic action was also observed with successive intravenous injections of YM-14673, once daily for 5 and 14 days in mice, suggesting that the drug induced no tolerance. In addition, there was evidence that the pituitary-thyroid axis was not necessary for the analeptic effects of YM-14673. In particular, it was noted that hypophysectomy did not reduce the antagonism by YM-14673 of pentobarbital-induced sleep and intracerebrally administered YM-14673 produced analeptic actions in mice. Pretreatment with atropine and baclofen antagonized the ability of YM-14673 to reduce sleep, induced by pentobarbital in mice. However, the analeptic action of YM-14673 was not reduced by the administration of haloperidol and phentolamine. These results suggest that YM-14673 produced facilitatory effects on the central nervous system, independent of an effect on the pituitary gland, and that the antagonizing effects by YM-14673 on the actions of pentobarbital may be affected by activation of the central cholinergic system as well as by inhibition of the GABA-ergic system.

Animals↗
PubMed1991

D1 agonist SKF 38393 antagonizes pentobarbital-induced narcosis and depression of hippocampal and cortical cholinergic activity in rats.

SKF 38393 (5 mg/kg), but not quinpirole, shortened the duration of loss of righting reflex produced in pentobarbital-narcotized rats. This effect was blocked by atropine (2 mg/kg), but not by atropine methylbromide, suggesting involvement of central cholinergic mechanisms. The analeptic effect was also blocked by SCH 23390 (0.2 mg/kg) or raclopride (2 mg/kg). SKF 38393 also increased sodium dependent high affinity choline uptake (HACU) in cortical and hippocampal synaptosomes that had been depressed by pentobarbital. SCH 23390 or raclopride prevented the SKF 38393 reversal of the depressed HACU, indicating that both D1 and D2 mechanisms were involved mediating the analeptic effect. These results provide neurochemical evidence that cortical and hippocampal D1-mediated cholinergic activation results in a behavioral arousal (analeptic) response. They also suggest that DA mechanisms may be involved in regulation of cortical and hippocampal cholinergic neurons.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1983

Morphine antagonizes pentobarbital-induced anesthesia.

Morphine was administered by the intracerebroventricular (i.c.v.) route to pentobarbital-anesthetized rabbits. Small doses of morphine (less than 150 micrograms) potentiated, but larger doses (greater than 250 micrograms) shortened, the duration of anesthesia. In naltrexone-pretreated animals, all doses of morphine employed acted only as an analeptic. Atropine, but not atropine methylbromide, blocked the analeptic effect of morphine, indicating that a central cholinergic mechanism was involved in this response. Tolerance to the analeptic effect was not evident. These results suggest that morphine exerts an arousal action which is usually masked by the dominant narcotic properties, but which becomes evident when administered intracerebroventricularly or in the presence of naltrexone.

Anesthesia↗
PubMedDate not supplied

Centrally administered vasopressin antagonizes pentobarbital-induced narcosis and depression of hippocampal cholinergic activity.

Intracerebroventricular (ICV) microinjection of arginine vasopressin (AVP) to pentobarbital-anesthetized rats produced shortening of the duration of narcosis. This analeptic effect was blocked by atropine, indicating the central cholinergic nature of the response. AVP also increased hippocampal sodium-dependent high affinity choline uptake activity that had been depressed by the barbiturate. The AVP analeptic effect was blocked by pretreatment with a V-1 (vasopressor), but not a V-2 (antidiuretic), vasopressin receptor antagonist. These results suggest that ICV AVP produces its analeptic effect by interacting with central V-1 receptors to activate a hippocampal cholinergic arousal system. The cholinergic arousal effect may be a factor in the memory enhancing property of AVP.

Acetylcholine↗
PubMed1999

Novel TRH analog improves motor and cognitive recovery after traumatic brain injury in rodents.

Thyrotropin-releasing hormone (TRH) and certain TRH analogs show substantial neuroprotective effects in experimental brain or spinal cord trauma but also have other physiological actions (autonomic, analeptic, and endocrine) that may be undesirable for the treatment of neurotrauma in humans. We developed a novel TRH analog (2-ARA-53a), with substitutions at the NH(2)-terminus and imidazole ring, that preserves the neuroprotective action of TRH-like compounds while decreasing or eliminating their autonomic, analeptic, and endocrine effects. Rats administered 2-ARA-53a (1.0 mg/kg, n = 17) intravenously 30 min after lateral fluid percussion brain injury showed marked improvement in motor recovery compared with vehicle-treated controls (n = 14). Treatment of mice subjected to moderate controlled cortical impact brain injury, at the same dose and time after trauma (n = 8), improved both motor recovery and cognitive performance in a water maze place learning task compared with vehicle-treated controls (n = 8). In injured rats, no autonomic or analeptic effects were observed with this compound, and endocrine effects were significantly reduced with 2-ARA-53a, in contrast to those found with a typical NH(2)-terminal-substituted TRH analog (YM-14673). These findings demonstrate that the neuroprotective effects of TRH-related compounds can be dissociated from their other major physiological actions and suggest a potential role for dual-substituted TRH analogs in the treatment of clinical neurotrauma.

Animals↗