Central nervous system ethanol affecting

As blood ethanol concentration rises above 18 mM (the legal intoxication limit is now defined as 0.08% in most states of the United States, which is approximately 18 mM), the brain and central nervous system are affected. Induction of CYP2E1 increases the rate of ethanol clearance from the blood, thereby contributing to increased alcohol tolerance. However, the apparent ability of a chronic alcoholic to drink without appearing inebriated is partly a learned behavior. 

Central nervous system depressants. Affect voluntary motor functions, causing loss of fine motor coordination, unconsciousness. Examples methanol, ethanol, ether. 

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). 

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). 

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. 

Buspirone causes less psychomotor impairment than diazepam and does not affect driving skills. The drug does not potentiate the central nervous system depressant effects of conventional sedative-hypnotic drugs, ethanol, or tricyclic antidepressants, and elderly patients do not appear to be more sensitive to its actions. Tachycardia, palpitations, nervousness, gastrointestinal distress, and paresthesias may occur more frequently than with benzodiazepines. Buspirone also causes a dose-dependent pupillary constriction. Blood pressure may be elevated in patients receiving MAO inhibitors. A number of buspirone analogs have been developed (eg, ipsapirone, gepirone, tandospirone) and are under study. 

The chronic effect of carbon disulfide and ethanol was examined by Opacka et al. (1984). Rats were exposed to 257 ppm of carbon disulfide for 5 hours a day, 6 days a week, for 11 months, and 10% ethanol (in water ad libitum for the last 3 months, control water ad libitum). Control rats were exposed to filtered air. The behavior, memory, and learning ability of the ethanol-fed rats were adversely affected compared to controls. Additional studies indicate biochemical alterations in the central nervous system and increased -glucuronidase activity ultrastructural studies show degeneration in the peripheral nervous system, particularly in the myelin sheath. These authors reported that the effects from combined exposures are greater than those from each substance alone. Wronska-Nofer et al. (1986) investigated the... 

Methanol, which has caused many fatalities when ingested accidentally or consumed as a substitute for beverage ethanol, is metabolically oxidized to formaldehyde and formic acid. In addition to causing acidosis, these products affect the central nervous system and the optic nerve. Acute exposure to a lethal dose causes an initially mild inebriation, followed in about 10-20 hours by unconsciousness, cardiac depression, and death, Subletal exposures can cause blindness from deterioration of the optic nerve and retinal ganglion cells. Inhalation of methanol fumes may result in chronic, low level exposure. 

Most, if not all, of the tissues and organs in the body are adversely affected by chronic ingestion of excessive amounts of alcohol, including the liver, pancreas, heart, reproductive organs, central nervous system, and the fetus. Some of the effects of alcohol ingestion, such as the psychotropic effects on the brain or inhibition of vitamin transport, are direct effects caused by ethanol itself. However, many of the acute and chronic pathophysiologic effects of alcohol relate to the pathways of ethanol metabolism (see Chapter 25). 

Al Martini is suffering from both short-term and long-term effects of ethanol on his central nervous system. Data support the theory that the shortterm effects of ethanol on the brain partially arise from an increase in membrane fluidity caused when ethanol intercalates between the membrane lipids. The changes in membrane fluidity may affect proteins that span the membrane (integral proteins), such as ion channels and receptors for neurotransmitters involved in conducting the nerve impulse. 

Alcohol, specifically ethanol (CH3CH2OH), is a mild depressant that affects your central nervous system. The specific biological effects are pretty complicated— some systems are enhanced by ethanol, others are inhibited. This combination of effects is why drinking can relax your muscles but also make you more animated. It may seem that alcohol lowers your inhibitions, but some experiments suggest this is a psychological effect and not a chemical one. 

Frequency and Duration of Exposure. The frequency and duration of exposure to toxic chemicals play an important role in toxicity. For many toxic chemicals, the adverse health effects associated with a single exposure are different from those associated with repeated exposures. A single exposure to benzene may cause central nervous system depression, while repeated exposures may cause leukemia. Infrequent exposure to ethanol affects the central nervous system while frequent exposure includes the liver as a target organ. 

Ethanol acts as a drug affecting the central nervous system. Its behavioral effects stem from its effects on the brain and not on the muscles or senses themselves. It is a depressant, and depending on dose can be a mild tranquilizer or a general... 

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