Drugs online research references
J Pharmacol Exp Ther. 1975 Aug;194(2):285-95.
Interactions of tricyclic antidepressants and barbiturates in barbiturate-tolerant and nontolerant rats.
Liu SJ, Huang CL, Waters IW.
Pretreatment of rats with tricyclic antidepressants, imipramine, desipramine, amitriptyline and nortriptyline, at two doses (5 and 25 mg/kg) 20 minutes before administration of barbiturate markedly reduced the latent period of the response to barbital and prolonged the sleeping time induced by pentobarbital (PB) and barbital. The effects were dose-dependent. The prolonged sleeping time produced by PB was associated with decreases in the rates of disappearance of PB from the brain and plasma. The effect of tricyclic antidepressants on PB hypnosis in PB-tolerant and nontolerant rats was apparently not related to change in central nervous system (CNS) sensitivity to PB, since at the time of awakening there were no significant differences in the concentrations of unmetabolized PB in either the plasma or brain of tricyclic antidepressant-treated animals as compared to controls. As barbital is not metabolized, potentiation of barbital hypnosis by tricyclic antidepressants must be attributable to a direct effect on CNS rather than on liver microsomal enzymes. Direct evidence was provided by the findings that amitriptyline accelerated the brain uptake of barbital and that amitriptyline-treated animals lost and recovered the righting reflex at brain barbital levels lower than those of controls. Rats made tolerant to the hypnotic effect of barbital also became tolerant, in varying degrees, to the hyposis-prolonging properties of tricyclic antidepressants. It is concluded that tricyclic antidepressants prolong PB sleeping time in PB-tolerant and nontolerant rats by inhibiting its biotransformation in the liver. The action of tricyclic antidepressants to prolong the hypnotic action of barbital in normal rats is related to their direct effects on CNS sensitivity to barbital, but such effects are makedly diminished after animals become tolerant to barbital.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1151759&dopt=Abstract
Pain. 1990 Nov;43(2):155-62.
Studies on the effects of antidepressant drugs on the antinociceptive action of morphine and on plasma morphine in rat and man.
Ventafridda V, Bianchi M, Ripamonti C, Sacerdote P, De Conno F, Zecca E, Panerai AE.
Department of Pharmacology, University of Milan, Italy.
In the rat we studied the effect of 3 tricyclic antidepressants: chlorimipramine, amitriptyline and nortriptyline, and the atypical antidepressant trazodone on pain thresholds when administered alone or together with morphine. Moreover, we evaluated the effect of the antidepressants on free morphine plasma concentrations both in the rat and in man. We observed that chlorimipramine and amitriptyline, two tricyclic antidepressants active on the serotoninergic system, induce analgesia and potentiate morphine analgesia in a dose-related fashion. The noradrenergic tricyclic nortriptyline and trazodone did not elicit analgesia and inconsistently affected morphine analgesia. In the rat, all drugs tested increased plasma concentrations of morphine with the exception of amitriptyline. In man, only chlorimipramine and amitriptyline increased the plasma concentration of the free opiate.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2087328&dopt=Abstract
Indian J Physiol Pharmacol. 1986 Jan-Mar;30(1):70-8.
Modification by tricyclic antidepressants of cortical EEG changes induced by clonidine in conscious rats.
Parale MP, Nayar U, Kulkarni SK.
The effects of various tricyclic antidepressants on clonidine-induced electroencephalographic changes were investigated in rats. The EEG pattern of conscious rats was recorded by means of bipolar electrodes, implanted chronically. Clonidine (50, 150 and 300 micrograms/kg) not only synchronized cortical EEG pattern but also evoked signs of behavioural depression within 15 min of its administration. Pretreatment with imipramine, desipramine, trimipramine, amitriptyline, nortriptyline and doxepin reduced clonidine-induced EEG synchrony without showing any effects per se. Acute treatment with tricyclic antidepressants failed to modify but, chronic treatment abolished the clonidine-induced behavioural depressive signs. Chronic administration of tricyclic antidepressants (10 mg/kg/day) evoked more pronounced antagonism of the EEG effects of clonidine. Yohimbine (200 micrograms/kg) pretreatment inhibited both, clonidine-induced EEG synchrony and behavioural effects. Guanfacine as well as B-HT 920, elicited clonidine-like effects on cortical EEG pattern and behaviour. The present data suggests that antagonism of clonidine-induced EEG synchronization in conscious animals could serve as a useful test for screening of antidepressant drugs.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3818034&dopt=Abstract
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