Central nervous system ethanol

Ethanol is classified for medical purposes as a central nervous system (CNS) depressant. Its effects—that is, being drunk—resemble the human response to anesthetics. There is an initial excitability and increase in sociable behavior, but this results from depression of inhibition rather than from stimulation. At a blood alcohol concentration of 0.1% to 0.3%, motor coordination is affected, accompanied by loss of balance, slurred speech, and amnesia. When blood alcohol concentration rises to 0.3% to 0.4%, nausea and loss of consciousness occur. Above 0.6%, spontaneous respiration and cardiovascular regulation are affected, ultimately leading to death. The LD50 of ethanol is 10.6 g/kg (Chapter 1 Focus On). 

Procarbazine causes myelosuppression, hypnotic and other effects on the central nervous system, e.g., vivid nightmares. Also, procarbazine causes a disulfiram like syndrome on ingestion of ethanol. 

Salicylism, or salicylic acid toxicity, is characterized by rapid breathing, tinnitus, hearing loss, dizziness, abdominal cramps, and central nervous system reactions. It has been reported with 20% salicylic acid applied to 50% of the body surface, and it has also been reported with use of 40 and 50% salicylic acid paste preparations [7]. The author has peeled more than 1,000 patients with the current 20 and 30% marketed ethanol formulations and has observed no cases of salicylism. 

Alcohol can affect the metabolism of trichloroethylene. This is noted in both toxicity and pharmacokinetic studies. In toxicity studies, simultaneous exposure to ethanol and trichloroethylene increased the concentration of trichloroethylene in the blood and breath of male volunteers (Stewart et al. 1974c). These people also showed "degreaser s flush"—a transient vasodilation of superficial skin vessels. In rats, depressant effects in the central nervous system are exacerbated by coadministration of ethanol and trichloroethylene (Utesch et al. 1981). 

Attempts to diminish the overall metabolism of trichloroethylene might be useful (e.g., hypothermia, mixed-function oxidase inhibitors, competitive inhibitors of trichloroethylene metabolism [i.e., P-450 substrates]), if instituted soon enough after trichloroethylene exposure. Catecholamines (especially beta agonists) act in concert with trichloroethylene, increasing the risk of cardiac arrhythmias. Hence, catecholamines should be administered to patients only in the lowest efficacious doses and for certain limited presentations of trichloroethylene poisoning. Ethanol should also be avoided because concurrent exposure to trichloroethylene and ethanol can cause vasodilation and malaise and may potentiate central nervous system depression at high dosage levels of either compound. 

A 3-year-old boy consumed a liquid from a container in the family garage He shows central nervous system (CNS) depression, acidosis, suppressed respiration, and oxalate crystals in the urine. Besides supportive and corrective measures, ethanol was administered to the child. 

Herbai sedatives and anxioiytics are a diverse group of plant drugs that commonly act as depressants of the central nervous system (CNS) (table 6.1). Pharmaceutical CNS depressants are used as anxiolytics, anti-epiieptics, sedatives, sleep-inducers (sedatives or hypnotics), general anesthetics, and recreationai drugs (e.g., ethanol) (table 6.2). CNS... 

Vasiliou V, Ziegler TL, Bludeau P, Petersen DR, Gonzalez FJ, et al. 2006. CYP2EI and catalase influence ethanol sensitivity in the central nervous system. Pharmacogenet Genomics 16 51-58. 

Olive ME. 2002. Interactions between taurine and ethanol in the central nervous system. Amino Acids 23(4) 345-357. 

Ingestion of ethanol acts on the central nervous system. In moderate amounts, it affects Judgment and lowers inhibitions. Higher concentrations cause nausea and loss of consciousness. Even at higher concentrations, it interferes with spontaneous respiration and can be fatal. 

Ethanol can increase the levels of many enzymes involved in metabolism of xenobiotics. Prolonged ethanol intake causes irreversible damage in the central nervous system and in the liver, resulting in marked decreased capacity for detoxification of xenobiotics and thereby increased sensitivity to a number of chemicals (KEMI 2003). 

As with other central nervous system depressants, the effects of benzodiazepines are additive with those of ethanol. Patients should be warned that ethanol-containing beverages may produce a more profound depression when taken simultaneously with a benzodiazepine. 

Ethanol (ethyl alcohol) has central nervous system depressant properties and is widely used to relieve anxiety and produce sedation. Although some medical practitioners occasionally prescribe an alcoholic beverage for relieving minor anxiety and inducing sleep, individuals frequently self-medicate with ethanol. Many individuals who abuse alcohol may have started using it to relieve symptoms of central nervous system disorders, such as anxiety and depression. 

Ethanol produces central nervous system depression over a wide range of doses. Its effects are additive or sometimes more than additive with other central nervous system depressants. Symptoms often associated with acute alcohol intoxication include increase in self-confidence, loss of inhibitions, euphoria, and loss of judgment. With increasing doses motor and intellectual impairment become prominent. Chronic abuse of ethanol leads to severe liver impairment (see Chapter 35). 

Sildenafil has other minor adverse effects, such as headache, nasal congestion, and flushing. There are no clinically significant drug interactions between sildenafil and apomorphine. Apomorphine, like sildenafil, is orally active. However, unlike sildenafil, it exerts its action through the central nervous system. Apomorphine can produce dizziness, nausea, pallor, and hypotension, and in the presence of ethanol, it purportedly increases... 

Central nervous system effects. Ethanol (60%) extract of the dried seed, administered orally to adults at a dose of 30 mL/per-son, increased acuteness of hearing. Water extract of the roasted seed, administered orally to adults, produced an increase in work performance. ... 

Central nervous system (CNS) depressant activity. Ethanol (95%) extract of the seed, administered orally to mice and rats at a dose of 50 mg/kg, was inactive° . 

Tolerance—decreased responsiveness to a drug following repeated exposure—is a common feature of sedative-hypnotic use. It may result in the need for an increase in the dose required to maintain symptomatic improvement or to promote sleep. It is important to recognize that partial cross-tolerance occurs between the sedative-hypnotics described here and also with ethanol (see Chapter 23)—a feature of some clinical importance, as explained below. The mechanisms responsible for tolerance to sedative-hypnotics are not well understood. An increase in the rate of drug metabolism (metabolic tolerance) may be partly responsible in the case of chronic administration of barbiturates, but changes in responsiveness of the central nervous system (pharmacodynamic tolerance) are of greater importance for most sedative-hypnotics. In the case of benzodiazepines, the development of tolerance in animals has been associated with down-regulation of brain benzodiazepine receptors. Tolerance has been reported to occur with the extended use of zolpidem. Minimal tolerance was observed with the use of zaleplon over a 5-week period and eszopiclone over a 6-month period. 

Disadvantages of the benzodiazepines include the risk of dependence, depression of central nervous system functions, and amnestic effects. In addition, the benzodiazepines exert additive central nervous system depression when administered with other drugs, including ethanol. The patient should be warned of this possibility to avoid impairment of performance of any task requiring mental alertness and motor coordination. In the treatment of generalized anxiety disorders and certain phobias, newer antidepressants, including selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs), are now considered by many authorities to be drugs of first choice (see Chapter 30). 

We reported the effects of ethanol extract of C. sativus and its purified components on the central nervous system in terms of learning behaviors in mice and the LTP in the dentate gyrus of hippocampus in anesthetized rats and in the CA1 region of rat hippocampal slices [11-13], This review also discusses the values of folk medicines in modulating apoptotic cell death, together with our recent data of crocin s effect on neuronal cell death. 

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