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PubMed2002

Therapeutic drug monitoring of racemic venlafaxine and its main metabolites in an everyday clinical setting.

When Efexor (venlafaxine) became available in Sweden, a therapeutic drug monitoring (TDM) service was developed in the authors' laboratory. This analytical service was available to all physicians in the country. From March 1996, to November 1997, 797 serum concentration analyses of venlafaxine (VEN) and its main metabolites, O-desmethylvenlafaxine (ODV), N-desmethylvenlafaxine (NDV), and N,O-didesmethylvenlafaxine (DDV) were requested. These samples, each of which was accompanied by clinical information on a specially designed request form, represented 635 inpatients or outpatients, comprising all ages, treated in a naturalistic setting. The first sample per patient, drawn as a trough value in steady state and with documented concomitant medication, was further evaluated pharmacokinetically (n = 187). The doses prescribed were from 37.5 mg/d to 412.5 mg/d. There was a wide interindividual variability of serum concentrations on each dose level, and the mean coefficient of variation of the dose-corrected concentrations (C/D) was 166% for C/D VEN, 60% for C/D ODV, 151% for C/D NDV, and 59% for C/D DDV. The corresponding CV for the ratio ODV/VEN was 110%. However, within patients over time, the C/D VEN and ODV/VEN variation was low, indicating stability in individual metabolizing capacity. Patients over 65 years of age had significantly higher concentrations of C/D VEN and C/D ODV than the younger patients. Women had higher C/D NDV and C/D DDV, and a higher NDV/VEN ratio than men, and smokers showed lower C/D ODV and C/D DDV than nonsmokers. A number of polycombinations of drugs were assessed for interaction screening, and a trend for lowered ODV/VEN ratio was found, predominantly with concomitant medication with CNS-active drug(s) known to inhibit CYP2D6.

Adolescent↗
PubMed2001

Successful use of cardiac allograft from serotonin antagonist intoxication.

BACKGROUND: Compromised organ donors are generally not accepted for heart transplantation (HT) despite the increasing number of critically ill patients on the waiting lists. By extending the donor criteria to include certain cases of intoxication, the organ shortage may be reduced. METHODS: The case of a successful orthotopic HT with an allograft from a donor poisoned by antidepressant overdose is presented. RESULTS: Early graft function was satisfactory with anteroseptal dyskinesis and an ejection fraction of 75% on echocardiography. The cardiac allograft recipient suffered some postoperative complications including gastrointestinal problems. The following period was up to now uneventful. Discharge from the intensive care unit was after 4 days. In-hospital stay was prolonged at 26 days. CONCLUSIONS: Because of limited myocardial toxicity, donor hearts from certain victims of antidepressant intoxication may be safely used for HT. Existing cardiac organ donor criteria must be reevaluated to maximise the available organ pool.

Adult↗
PubMed2003

Role of CYP2D6 in the stereoselective disposition of venlafaxine in humans.

CYP2D6 is involved in the O-demethylation metabolic pathway of venlafaxine in humans. In this study, we investigated whether this isozyme is stereoselective. Plasma samples from seven CYP2D6 extensive metabolizers (EMs) and five CYP2D6 poor metabolizers (PMs), collected during a period without and with coadministration of quinidine, were analysed. Subjects were administered venlafaxine hydrochloride 18.75 mg orally every 12 h for 48 h on two occasions (1 week apart); once alone and once during the concomitant administration of quinidine sulphate every 12 h. Blood and urine samples were collected under steady-state conditions over one dosing interval (12 h). The present results show that, although CYP2D6 catalyses the O-demethylation of both enantiomers of venlafaxine, it displays a marked stereoselectivity towards the (R)-enantiomer. The oral clearance of (R)-venlafaxine was found to be nine-fold higher in EMs compared to PMs [median (range) 173 (29-611) l/h versus 20 (16-24) l/h, P < 0.005], while it was two-fold higher for (S)-venlafaxine [73 (32-130) l/h versus 37 (21-44) l/h, P < 0.05]. In EMs, quinidine decreased (R)- and (S)-venlafaxine oral clearance by 12-fold ( 0.05) and four-fold ( 0.05), respectively. In contrast, quinidine did not have any effects on renal clearance of (R)-venlafaxine [4 (2-10) l/h for venlafaxine alone versus 5 (0.6-7) l/h for venlafaxine + quinidine] and of (S)-venlafaxine [4 (1-7) l/h for venlafaxine alone versus 3 (0.4-6) l/h for venlafaxine + quinidine]. The coadministration of quinidine to EMs resulted in an almost complete inhibition of the partial metabolic clearance of (R)-venlafaxine to O-demethylated metabolites [127 (10-493) l/h down to 1 (0.1-3) l/h, 0.05], while a seven-fold reduction was measured for (S)-venlafaxine [47 (14-94) l/h versus 7 (1-19) l/h, 0.05]. In PMs, coadministration of quinidine did not significantly change oral clearance and partial metabolic clearance of (R)- and (S)-venlafaxine to its various metabolites. In contrast, data obtained on the partial metabolic clearance of (R)- and (S)-venlafaxine to N-demethylated metabolites, a reaction which is mediated by CYP3A4, suggest a lack of stereoselectivity of this enzyme.

Administration, Oral↗
PubMed1997

Potentiation of the time-dependent, antidepressant-induced changes in the agonistic behaviour of resident rats by the 5-HT1A receptor antagonist, WAY-100635.

Acute and chronic antidepressant drug treatments respectively decrease and increase the aggressive behaviour of resident rats during encounters with unfamiliar conspecifics. We have now examined the effect of the 5-hydroxytryptamine1A receptor antagonist, WAY-100635, on fluoxetine-, paroxetine- or venlafaxine-induced changes in aggression. WAY-100635 (0.1 mg/kg), which did not modify behaviour when given alone, potentiated the venlafaxine (5.54 mg/kg)-induced reduction in aggression after acute treatment and, during chronic treatment, accelerated the fluoxetine (0.34 mg/kg/day)-induced increase in aggression, from day 5 to day 2. A similar change in time course was seen with paroxetine (0.33 mg/kg/day), although the increase in aggression was smaller. Venlafaxine (5.54 mg/kg/day, alone or co-administered with WAY-100635) increased aggression by day 2. During chronic treatment, therefore, venlafaxine, at the dose used, had a more rapid onset of action than either fluoxetine or paroxetine, whereas the fluoxetine- and paroxetine-, but not the venlafaxine-, induced increase in aggression was accelerated by WAY-100635. These studies further support the hypothesis that selective blockade of the 5-hydroxytryptamine1A receptor augments the effects of antidepressant drugs in an animal model predictive of antidepressant activity, presumably by concomitant blockade of the somatodendritic 5-hydroxytryptamine1A autoreceptor-mediated negative feedback system of serotonergic neurones.

Agonistic Behavior↗
PubMed2000

Serotonin, noradrenaline and cognitive function: a preliminary investigation of the acute pharmacodynamic effects of a serotonin versus a serotonin and noradrenaline reuptake inhibitor.

Comparisons of the behavioural side-effect profiles of antidepressants that inhibit either serotonin or both serotonin and noradrenaline reuptake, may reveal differences in cognitive and psychomotor functions, which may be attributed to their relative pharmacological selectivity for potentiating monoamine neurotransmission in the central nervous system. The aim of the present study was to determine the acute pharmacodynamic effects of citalopram and venlafaxine, on cognitive and psychomotor performance. Nine healthy male volunteers received a single clinical dose of citalopram, venlafaxine or amitriptyline (positive control) in a double-blind placebo-controlled design. Cognitive and psychomotor tests and a subjective measure of sedation were examined before and 1, 2 and 4 hours after drug administration. Citalopram improved psychomotor responses to sensory stimuli and sustained attention, with significant decreases in movement times of the choice reaction time test and an increase in critical flicker fusion threshold. Venlafaxine did not affect performances on any of the cognitive or psychomotor tests examined. Differences may be related to relative potencies of the compounds for monoamine reuptake inhibition.

Adult↗
PubMed2002

Differing effects of the cannabinoid agonist, CP 55,940, in an alcohol or Tween 80 solvent, on prepulse inhibition of the acoustic startle reflex in the rat.

It has been suggested that cannabinoid agonists increase dopamine (DA) transmission in the mesolimbic dopamine system. However, evidence for such an effect is inconsistent. Prepulse inhibition (PPI) of the acoustic startle reflex is a behavioural paradigm that is modulated by an increase of mesolimbic dopamine. This study sought to ascertain whether or not a cannabinoid agonist, CP 55,940, mimicked the effects of amphetamine (a drug which increases dopamine release) on PPI. The first experiment measured the PPI of 16 male Wistar rats injected (i.p.) with different doses of CP 55,940 in a Latin-square design. A second experiment replicated the effects of the first experiment in a between-subjects design, and also examined the effects of using a 5% alcohol solution as a solvent for cannabinoid agonists, in comparison to the more inert detergent, Tween 80. In both experiments, CP 55,940 in Tween 80 significantly reduced basal activity, increased startle onset latencies and increased PPI, effects opposite to those of amphetamine. These results suggest that the net behavioural effects of cannabinoids are opposite to those of amphetamine. In addition, it was found that 1 ml/kg of a 5% alcohol solution has significant behavioural effects on its own, and reverses the effects of CP 55,940 on PPI.

Acoustic Stimulation↗
PubMed2004

Behavioral effects of cannabinoids show differential sensitivity to cannabinoid receptor blockade and tolerance development.

This study compared the potency and efficacy of the cannabinoids delta-tetrahydrocannabinol (delta-THC), HU-210, WIN 55,212-2 and CP 55,940 in suppressing food-reinforced operant behavior, increasing reaction latency in a hot-plate test and inducing hypothermia, and tested whether these behavioral effects induced by CP 55,940 showed differential sensitivity to the cannabinoid CB1 receptor antagonist SR141716A, and to tolerance development. After acute i.p. administration to rats, operant behavior was more potently affected than reaction latency and body temperature, but the order of potency of the different drugs was similar across the tests: HU-210<CP 55,940<WIN 55,212-2=delta-THC. SR141716A blocked the hypothermic and analgesic effects more potently/efficiently than the response-rate suppressive effect of CP 55,940. After repeated administration of CP 55,940, the extent and speed of tolerance development was most pronounced in the hypothermia test, and least pronounced in the operant test. It is concluded that the more the behavioral effect induced by a cannabinoid receptor agonist is situated at the left-hand side of the dose-spectrum, the more the effect is resistant to blockade by a cannabinoid receptor antagonist and to the development of tolerance. The possible consequence of this observation for the therapeutic use of cannabinoids is discussed.

Analgesics↗
PubMed2004

Partial agonist-like profile of the cannabinoid receptor antagonist SR141716A in a food-reinforced operant paradigm.

Both cannabinoid CB1 receptor agonists, such as delta-tetrahydrocannabinol (delta-THC), CP 55,940 and WIN 55,212-2, and the antagonist/inverse agonist SR141716A, dose-dependently suppress operant behavior. The present study investigated to what extent combined i.p. application of SR141716A with these cannabinoids resulted in mutually antagonistic effects, in additive effects, or in no interactive effects on operant responding in rats trained in a fixed-ratio 10, food-reinforced 10-min procedure. Pretreatment with SR141716A either had no effect on (at 0.3-1mg/kg), or partially blocked (at 3 mg/kg), the inhibitory effects on responding induced by delta-THC (3-5 mg/kg) and CP 55,940 (0.03-0.2 mg/kg). Interestingly, while 3 mg/kg SR141716A induced moderate inhibitory effects on operant responding, its combination with either agonist resulted in the same level of inhibitory activity on responding as that obtained by SR141716A when tested alone. Pretreatment with a low dose of CP 55,940 (0.01 mg/kg) or WIN 55,212-2 (0.3 mg/kg) did not affect response inhibition induced by SR141716A. Combination of SR141716A (0.5 and 1mg/kg) with delta-THC (3 mg/kg) resulted in the same level of response inhibition, independently of whether SR141716A was given 5 min before or 15 min after delta-THC. Although alternative explanations are conceivable, the data may indicate that SR141716A is a partial agonist at those cannabinoid receptors mediating the response-rate suppressive effects of cannabinoids.

Animals↗
PubMed2004

Involvement of 5-HT1A receptors in behavioural effects of the cannabinoid receptor agonist CP 55,940 in male rats.

We have studied the possible interaction between the cannabinoid receptor agonist CP 55,940 (1 and 50 microg/kg) and the 5-HT1A receptor antagonist WAY 100635 (1 mg/kg) in the modulation of plus-maze and holeboard activity in Wistar adult male rats. In the plus-maze, the higher dose of CP 55,940 induced an anxiogenic-like effect, whereas the lower dose induced anxiolytic-like responses. The 5-HT1A antagonist, which was silent in this test, attenuated the anxiogenic, but not the anxiolytic, effect of CP 55,940. In the holeboard, the higher dose of CP 55,940 significantly decreased head-dipping duration, and WAY 100635, which did not affect exploratory head-dipping when administered alone, antagonized this effect. The administration of WAY 100635 significantly increased grooming behaviour, and this effect was inhibited by the two doses of CP 55,940, which did not exert any effect, per se, on this parameter. We provide the first evidence implicating 5-HT1A receptors in anxiety-related behavioural responses to a cannabinoid agonist.

Animals↗
PubMed2005

Behavioural and neuroendocrine effects of cannabinoids in critical developmental periods.

The present article focuses on psychoneuroendocrine effects of cannabinoids in developing animals, with special emphasis on the perinatal, periweanling and periadolescent periods. We describe and discuss published data dealing with acute and long-term effects of exposure to cannabinoid agonists in such critical periods. Human studies have demonstrated that the consumption of marijuana by women during pregnancy affects the neurobehavioural development of their children. Investigations using animal models provide useful information for a better understanding of the long-lasting deleterious consequences of cannabis exposure during pregnancy and lactation. The increasing use of cannabis among adolescents and its associated public health problems have led to a parallel increase in basic research on appropriate animal models. Chronic administration of cannabinoid agonists during the periadolescent period causes persistent behavioural alterations in adult animals. Some of these alterations may be related to a possible increased risk of psychosis and other neuropsychiatric disorders in early onset cannabis users.

Animals↗
PubMed2005

The role of CB1 receptors in sweet versus fat reinforcement: effect of CB1 receptor deletion, CB1 receptor antagonism (SR141716A) and CB1 receptor agonism (CP-55940).

It is well established that Cannabis sativa can increase appetite, particularly for sweet and palatable foods. In laboratory animals, cannabinoid CB1 receptor antagonism decreases motivation for palatable foods, and most recently, the CB1 receptor antagonist SR141716A, or rimonabant (Acomplia), was reported to produce weight loss in obese human subjects. Indeed, the endocannabinoid system plays a select role in the rewarding properties of palatable foods, and this is well characterized in laboratory animals with sweet sucrose solutions. In the present study, CB1 knockout mice (CB1 KO) and wild-type littermate mice (WT) were trained to respond for a complex sweet as well as a pure fat reinforcer under a progressive ratio (PR) schedule, to determine whether motivation to consume different palatable foods is tonically regulated by CB1 receptors. To assess sweet reinforcement, several concentrations of the liquid nutritional drink, Ensure, were presented under the PR schedule. For fat reinforcement, several concentrations of corn oil (emulsified in 3% xanthan gum) were made available. Additionally, to compare the result of genetic invalidation of the CB1 receptor to antagonism of the CB1 receptor system, the effect of SR141716A (3.0 mg/kg) on responding for Ensure and corn oil were also assessed using the PR schedule. We also assessed the effect of the CB1 agonist CP-55940 (30 microg/kg) on responding for Ensure and corn oil. CB1 KOs took significantly longer to acquire operant responding maintained by Ensure, and responding for Ensure under the PR schedule was significantly reduced in CB1 KOs as well as in WTs pretreated with SR141716A, as compared to WT controls. Additionally, pretreatment with the CB1 agonist CP-55940 increased responding for Ensure. In contrast, responding for corn oil during acquisition and under the PR schedule was not significantly different in CB1 KOs versus wild-type mice. However, SR141716A did reduce responding for corn oil in WTs, and CP-55940 significantly increased responding for corn oil. Taken together, these results suggest that CB1 receptors are preferentially involved in the reinforcing effects of a complex sweet, as compared to a pure fat, reinforcer. These data also suggest, however, that antagonism of CB1 receptors with SR141716A is sufficient to attenuate the reinforcing effect of Ensure and corn oil, while activation of the central CB1 system is sufficient to enhance Ensure and corn oil reinforcement.

Animals↗
PubMed2005

Persistent anxiogenic effects of a single or repeated doses of cocaine and methamphetamine: interactions with endogenous cannabinoid receptor ligands.

As persistent behavioural changes, such as increased anxiety-related behaviours, can be predicted based on the phenomenon of psychostimulant-induced neuronal plasticity, the time course (3-, 5- and 10-day time points) of the effects of both a single and repeated (daily for 7 days) i.p. administrations of cocaine (COC) and methamphetamine (MA) on anxiety-related behavioural symptoms in the elevated plus-maze test were examined in mice. Furthermore, based on the reported interactions between brain dopamine versus cannabinoid (CB) receptors and the contribution of CB receptors to the occurrence of persistent anxiety-related behavioural symptoms, the interactions of the agonist CP 55940 (CP) and the endogenous ligands anandamide (arachidonylethanolamide: AEA), 2-arachidonylglycerol (ARA), N-arachidonyldopamine (NADA), noladin ether (NL), and virodhamine (VA) with the COC- or MA-induced anxiety-related behaviours were also studied. In both an acute experiment using a single COC (30 mg/kg) or MA (4 mg/kg) dose and a chronic experiment using repeated COC (15 mg/kg) or MA (2 mg/kg) doses, anxiety-related behavioural symptoms were observed similarly at 3- and 5-day time points, but disappeared at the 10-day time point. Among the CB ligands, the agonists CP, AEA, ARA, NADA, and NL provided strong protective effects against each parameter at 3- and 5-day time points. Therefore, it was concluded that both COC and MA caused persistent anxiety-related behavioural symptoms following both a single and repeated treatments. Since these anxiogenic effects were attenuated by the endogenous CB agonists, the involvement of brain CB receptors was suspected.

Analysis of Variance↗
PubMed2005

Behavioral pharmacological properties of a novel cannabinoid 1',1'-dithiolane delta8-THC analog, AMG-3.

Newly developed cannabinoids may hold the promise of the development of useful and safe drugs. This study aimed to investigate the behavioral effects of the novel 1',1'-dithiolane delta8-HC analogue AMG-3, a cannabinomimetic molecule with high affinity for CB1/CB2 receptors. This analog was chosen for its binding affinity to these receptors, which is higher than that reported for delta8-tetrahydrocannabinol (delta8-THC). Behavioral responses were assessed after the administration of AMG-3 (1, 2, 4, 8 mg/kg, i.p.) in the open field, on the bar test, on the hot plate and in the intracranial self-stimulation procedure. AMG-3 increased the reactivity time on the hot plate in a dose- and time-dependent manner, indicating a long-lasting analgesic effect (at least 24 h). The substance was found dose-dependently to decrease spontaneous motor activity and to induce catalepsy, particularly at the highest dose (8 mg/kg). AMG-3 did not affect the rewarding value of intracranial self-stimulation, except to increase the reward threshold at the highest dose (8 mg/kg). The effects of the highest dose of AMG-3 on spontaneous activity and on the self-stimulation paradigm were completely reversed by pre-treatment with the CB1 receptor antagonist AM-251. These findings indicate that the administration of AMG-3 to rats elicits a specific behavioral profile, most probably associated with the activation of CB1 receptors and without effects indicating abuse potential.

Animals↗
PubMed1996

Canventol inhibits HIV-1 replication by Tat-induced Tar-independent mechanism.

SUMMARY: Canventol (2-isopropyl-4-isopropyldencyclohex-2-ene-l-ol), a blocker of tumor necrosis factor alpha (TNF-alpha) release, inhibits human immunodeficiency virus type (HIV-1) production in chronically and acutely infected cells. This effect of Canventol on virus replication could be correlated with its inhibitory influence on necrosis factor (NF)-kappa B activation and HIV-1 long terminal repeat (LTR)-driven reporter gene expression in Jurkat cells and these could be overcome by the administration of TNF-alpha. Canventol inhibits activation of the promoter by the viral protein Tat through a TAR-independent mechanism. The HIV-1 promoter is synergistically upregulated when both the TAR-independent and the TAR-dependent modes of Tat action are in operation. Tat-induced downstream events, such as the production of cytokines like TNF-alpha and NF-kappa B activation, are central for this upregulation. Inhibitors of the respective modes of action of Tat downregulate HIV-1 LTR activation and virus replication.

Antiviral Agents↗
PubMed1998

Inhibition of HIV-1 replication by combination of a novel inhibitor of TNF-alpha with AZT.

The small molecule S9a was derived from an established tumor necrosis factor-alpha (TNF-alpha) inhibitor (Canventol) by replacement of the isopropylidine group with a phenyl ring. S9a at 10 to 100 nM inhibited HIV production as potently as 3'-azido-3'-deoxythymidine (AZT), an inhibitor of viral reverse transcriptase. Furthermore, S9a and AZT in combination, at noncytoxic concentrations strongly inhibited HIV-1 replication that was more than additive and substantially prolonged the appearance of virus both in acutely infected CD4+ lymphocytes (SupT) in culture and in peripheral blood mononuclear cells (PBMCs) infected with a primary HIV-1 isolate. S9a inhibited TNF-alpha promoter-driven reporter gene activity. It was proposed that the mechanism of antiviral action of S9a was on the host cell, by blocking TNF-alpha transcription via a Tat-induced tar-independent loop, which decreases downstream NF-kappaB activation of HIV-1 long terminal repeat (LTR). S9a was superior to the first generation compound Canventol, which was superior to the natural compound sarcophytol A, demonstrating that further structure-based enhancement of potency of these compounds is feasible. This study suggests a therapeutic approach against AIDS by application of two drugs, one against a cellular and the other a viral target, which may provide an approach to the problem of frequent emergence of resistant variants to combinations of drugs that target only HIV genes.

Anti-HIV Agents↗
PubMedDate not supplied

Efficacy of venlafaxine for the long term treatment of chronic pain with associated major depressive disorder.

BACKGROUND: This was an open-label, single-center study of the long-term efficacy and effectiveness of venlafaxine extended release (XR) in the treatment of chronic pain and depression in outpatients. All patients have been diagnosed with major depressive disorder (MDD) of various types, with or without chronic pain, and had previously failed treatment with either tricyclic antidepressants (TCAs) or selective serotonin reuptake inhibitors (SSRIs). METHODS: Efficacy of treatment was determined using the 21-item Hamilton Rating Scale for Depression (HAMD-21), the Visual Analogue Scale (VAS) for the evaluation of pain, and a 12-item quality of life scale (QOL). Patients were treated in an unblended open trial for 1 year with 150 mg or more of venlafaxine XR once daily. RESULTS: After 1 year of treatment, 21-item Hamilton Rating Scale for Depression, Visual Analogue Scale, and quality of life scores were significantly improved from permanent baseline scores. CONCLUSION: These data show long-term efficacy and effectiveness of venlafaxine XR, a serotonin (5-HT) and norepinephrine (NE) and dopamine (DA) reuptake inhibitor antidepressant agent, having analgesic properties.

Adult↗
PubMed2000

Seizure activity and safety in combined treatment with venlafaxine and ECT: a pilot study.

Some authors have described the combined use of ECT and psychotropic drugs, emphasizing possible interactions and synergisms of this combined therapy. We are unaware of reports of the concurrent use of the new antidepressant venlafaxine with ECT. The goals of our study were to assess the possible effects of venlafaxine on seizure length during ECT and the possible cardiovascular effects of this combined treatment. Nine severely ill, depressed patients were treated simultaneously with bilateral ECT and venlafaxine 150 mg/day and were compared with nine control, depressed subjects taking tricyclic antidepressants (TCA) and ECT. No patients had prolonged seizures and no spontaneous/tardive seizures outside ECT were observed. With regard to mean seizure length, no statistically significant differences were observed between the control group and the venlafaxine group. Neither significant increases in arterial blood pressure nor electrocardiographic recording abnormalities were found in venlafaxine patients when compared with the tricyclic group. Even though the small number of patients used is a significant limitation of this study, we found that combined venlafaxine and ECT appears to be safe when used in depression.

Adult↗
PubMed2001

The combined use of bupropion, lithium, and venlafaxine during ECT: a case of prolonged seizure activity.

There is limited literature addressing the safety of administering electroconvulsive therapy (ECT) to patients concomitantly receiving bupropion monotherapy or in combination with other drugs that may alter the seizure threshold. We describe a prolonged seizure occurring during the first treatment of a course of ECT in an adult patient receiving long-term bupropion therapy, lithium, and venlafaxine.

Antidepressive Agents, Second-Generation↗