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"Ethanol withdrawal symptoms and ethanol-induced neuropathology Effects od dexmedetomidine treatment and aging Acta Universitati
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Saatavuus: Noin 5-8 arkipäivää
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"ETHANOL WITHDRAWAL SYMPTOMS AND ETHANOL-INDUCED NEUROPATHOLOGY EFFECTS OD DEXMEDETOMIDINE TREATMENT AND AGING ACTA UNIVERSITATI

Kirjailija:
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Kieli:
Englanti
Sivumäärä:
8840 sivua
Julkaisuvuosi:
ISBN:
9789514466397

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Arvioimme, että tuote lähetetään meiltä noin 5-8 arkipäivässä (17.07-22.07.2020).
"Ethanol withdrawal symptoms and ethanol-induced neuropathology Effects od dexmedetomidine treatment and aging Acta Universitatizoom

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Chronic ethanol exposure has been shown to cause degenerative changes in several areas of the brain, including cerebral cortex, hippocampus, cerebellum and brainstem, and also in the peripheral nervous system. Ethanol-induced neuronal degeneration is multifactorial in origin, and changes in several neurotransmitter systems during chronic ethanol exposure have been reported. Overactivity of the noradrenergic neurotransmission has been reported in both the central and the peripheral nervous system. In previous studies prolonged noradrenergic overactivity has been supposed to contribute to the morphological and functional degeneration of rat peripheral sympathetic nervous system. Aging has been suggested to enhance the ethanol-induced degenerative changes in the CNS. Ethanol withdrawal syndrome is the result of a cessation or reduction of a heavy, prolonged ingestion of alcohol. Alcoholics commonly undergo repeated withdrawal episodes. Even a single withdrawal episode has been reported to cause neurodegenerative alterations, and intermittent ethanol exposure with repeated withdrawal periods has been shown to be more harmful to neurons than continuous exposure. Overactivity of the noradrenergic nervous system has been shown to be one of the central mechanisms of the ethanol withdrawal syndrome. In the withdrawal phase, the noradrenergic overactivity may result, at least in part, from a reduced sensitivity of á2-adrenergic receptors. Aging has been reported to increase the severity of ethanol withdrawal syndrome. The aim of this study was to investigate the effects of dexmedetomidine (DEX), a selective and potent á2-adrenergic agonist, on the ethanol withdrawal syndrome. The effects of DEX were compared with those of diazepam and propranolol, drugs presently used in the clinical treatment of ethanol withdrawal. The possible neuroprotective effects of DEX on ethanol-induced neuronal degeneration were studied in the peripheral sympathetic neurons of the superior cervical ganglion (SCG) during a 12-day ethanol exposure and in the central adrenergic neurons of the locus coeruleus (LC) during a five-week intermittent ethanol exposure. The effects of aging on the severity of ethanol withdrawal symptoms and ethanol-induced neurodegeneration in the rat were studied during a five-week intermittent ethanol exposure. DEX significantly relieved the ethanol withdrawal syndrome in the rat, when measured as the sum score of the three most specific symptoms (rigidity, tremor, irritability). The efficiency of DEX in the treatment of ethanol withdrawal symptoms seemed to be comparable to the effect of diazepam. During the 5-week intermittent ethanol exposure, the effect of DEX on ethanol withdrawal symptoms seemed to remain unchanged or even improve during repeated withdrawal periods. DEX was shown to have neuroprotective effects on ethanol-induced degeneration in both the peripheral and the central nervous system. Aging did not significantly affect the severity of ethanol withdrawal symptoms or ethanol-induced loss of LC neurons. In conclusion, DEX seems to be an interesting new alternative in the treatment of the ethanol withdrawal syndrome, especially with regard to its potential neuroprotective effects.




Asiasanat: alkoholinkäyttö etanoli hermosto vauriot vieroitusoireet lääkehoito ikääntyminen
Tuoteryhmä: Suomalaiset kirjat


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