Use of high-performance liquid chromatography with diode-array detection after a primary drug screening in patients admitted to the emergency department.

Two hundred fifty samples of patients admitted to the Emergency Department at the Hospital Municipal de Urgencias, Córdoba, Argentina for a drug screening by HPTLC, FPIA, spectrophotometric methods, and HPLC/DAD were randomly selected. The rate of positive screens was 34.0% with the following rate distribution: 12.0% alcohol, 13.6% nonsteroid antiinflammatory drugs (NSAIDs), 2.0% anticonvulsants, 0.8% barbiturates, 0.4% narcotics, 0.4% antidepressants, 2.8% cocaine, and 2.0% cannabinoids. Psychoactive drugs (alcohol, cocaine, and cannabinoids) were detected in 43.9% of the patients admitted for traffic accidents, namely 35.71% alcohol, 2.38% alcohol-cocaine, 2.38% alcohol-cannabinoids, 2.38% cocaine-cannabinoids, and 2.38% alcohol-cocaine-cannabinoids. These results help identify the trend of use and/or abuse of drugs and its relationship with different causes of admission (accidents, overdose, and other pathologies), age, and gender.

A single exposure to restraint stress induces behavioral and neurochemical sensitization to stimulating effects of amphetamine: involvement of NMDA receptors.

Evidence indicates that repeated exposure to stressful events sensitizes the motor and addictive effects of drugs of abuse in rats. Regarding a single exposure to one restraint stress, previous findings have shown that it is sufficient to induce behavioral sensitization to stimulating and reinforcing properties of abuse drugs (e.g., amphetamine and morphine), as measured by locomotor activity and conditioned place preference, respectively. It is well known that enhanced dopaminergic neurotransmission in the nucleus accumbens and striatum plays a critical role in the development and/or expression of repeated stress-induced or drug-induced sensitization. In addition, involvement of NMDA receptors has been implicated in its development. However, whether sensitization induced by a single restraint stress exposure represents the same neurobiologic phenomenon is unknown. We studied the following issues: (a) influence of a single restraint exposure on the stimulating effects of amphetamine on dopamine release by microdialysis from striatum and (b) involvement of glutamatergic pathways, specifically those innervating striatum, on stress-induced sensitization to amphetamine, by administering MK-801 ip (0.1 mg/kg) or intrastriatally (1 microg/0.5 microL) previous to an acute restraint stress. For microdialysis studies (a) or intrastriatal administration of MK-801 (b), Wistar rats (250-330 g) were implanted stereotactically under anesthesia with a guide cannula in the striatum. After 2 days, animals were immobilized for 2 hours in a Plexiglas device. Control animals remained in their home cages. The following day we evaluated the stimulating effect of amphetamine on (a) dopamine release from striatum or (b) locomotor activity. In studies (a), dialysis probes were inserted into the guide cannula, and baseline dopamine levels were collected for 2 hours before a challenge of amphetamine (1.5 mg/kg i.p.). Dialysates were then collected by 3 hours. Amphetamine challenge induced a significantly higher increase in dopamine release and locomotor activity in animals previously subjected to one restraint stress exposure, relative to that observed in the no-restraint stress group. MK-801 administered i.p. or intrastriatally blocked the restraint stress-induced sensitization to amphetamine. First, our results point out that a single restraint stress exposure is a pertinent stimulus to induce sensitization of amphetamine's stimulating effects on dopaminergic neurotransmission in the striatum. Secondly, NMDA-glutamatergic receptors, specifically those placed in the striatum, are implicated in the development of stress restraint-induced sensitization.

Influence of different antidepressant drugs on the effect of chronic variable stress on restraint-induced dopamine release in frontal cortex.

The aim of this study was to evaluate the influence of an early chronic variable stress procedure (CVS) associated or not with repeated administration of various antidepressants on cortical restraint-induced dopamine (DA) release in vivo. Animals were subjected to the CVS schedule and one day after submitted to persistent administration with vehicle, desipramine (DMI, 10 mg/kg, i.p.), fluoxetine (FLU, 10 mg/kg, i.p.) or phenelzine (PHE; 10 mg/kg, i.p.) and later on exposed to a 60-min restraint period. In addition, we also explored the effect of acute administration of these antidepressants on cortical DA overflow in response to restraint in CVS treated rats. A higher increase in cortical DA release in response to restraint was observed in CVS animals as compared with those without previous CVS. Persistent, but not acute, administration with DMI, FLU and PHE blocked the sensitized output induced by restraint following CVS exposure.

Chronic amphetamine facilitates immunosuppression in response to a novel aversive stimulus: reversal by haloperidol pretreatment.

The effect of chronic d-amphetamine sulfate (AMPH) treatment (nine daily injections, 2 mg/kg i.p.) on subsequent foot shock stress-induced immunological response was investigated. In addition, the potential role of a dopaminergic (DA) mechanism in the development of chronic AMPH-induced changes in stress-influenced immune responses was characterized. Exposure to foot shock stress decreased the percentage of T-lymphocytes, and reduced the delayed-type hypersensitivity reaction (DTH) in chronically AMPH-pretreated rats relative to vehicle-treated controls. Both of those stress-induced immunosuppressive responses were no longer evident when AMPH-pretreated rats were injected with haloperidol (HAL, 1 mg/kg i.p.) 30 min prior to each daily AMPH injection. The present findings are indicative of a modulatory role for dopamine in the facilitating process induced by AMPH on stress-induced immunosuppressive effects.