Late cerebral embolization after emboli-protected carotid artery stenting.

Carotid artery stenting (CAS) is nowadays considered as alternative therapeutic option to carotid endarterectomy for patients suffering from carotid artery disease. Recent studies and meta-analyses have demonstrated equal performance of carotid stenting to endarterectomy as regard as the overall adverse events (death/stroke rates), especially when periprocedural myocardial infarction and nerve pulses are also included. However, carotid stenting was inferior to endarterectomy when compared in terms of acute and late embolic events. In the present review, we collect all studies available in the published literature regarding the late embolic events. We mainly attempted to gather data regarding the silent embolic events occurring after the acute post-procedural period. We analyzed the results and reported the incidence of the problem. Finally, we aimed to identify possible causes and propose effective solutions to reduce the incidence of late embolic events.

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.