Ethanol is a general central nervous system depressant, producing sedation and even sleep at higher doses. The degree of this depression is proportional to its concentration in the blood; however, this relationship is more predictable when ethanol levels are rising than three or four hours later, when blood levels are the same but ethanol levels are falling. This variance occurs because during the first fifteen or twenty minutes after an etha-nol dose, the peripheral venous blood is losing etha-nol to the tissues while the brain has equilibrated with arterial blood supply. Thus, brain levels are initially higher than the venous blood levels, and since all blood samples for ethanol determinations are taken from a peripheral vein, the ethanol con centrations are appreciably lower than a few hours later, when the entire system has achieved equilibrium.
The reticular activating system of the brain stem is the most sensitive area to ethanol's effects; this accounts for the loss of integrative control of the brain's higher functions. Anecdotal reports of a stimulating effect, especially at low doses, are likely due to the depression of the mechanisms that normally control speech and other behaviors that evolved from training or prior experiences. However, there may be a genetic basis for this initial stimulating effect, since rodents differing genetically show differences in the degree of initial stimulation or excitement. Upon drinking a moderate amount of ethanol, humans may quickly pass through the ''stimulating'' phase. Memory, the ability to concentrate, and insight are affected next whereas confidence often increases as moods swing from one extreme to another. If the dose is increased, then neuromuscular coordination becomes impaired. It is at this point that drinkers may be most dangerous, since they are still able to move about but reaction times and judgment are impaired—and sleepiness must be fought. The ability to drive an automobile or operate machinery is compromised. With higher doses, general (sleep) or surgical (unconsciousness) anesthesia may develop, but respiration is dangerously depressed.
Ethanol is believed by many to have a number of medicinal (therapeutic) uses; these are mostly based on anecdotal reports and have few substantiated claims. One example of a well-known but misguided use is to treat hypothermia—exposure to freezing conditions. Although the initial effects of an alcoholic beverage appear to ''warm'' the patient, ethanol actually dilates blood vessels, causing further loss of body heat. Another example is its effects on sleep— it is believed that a nightcap relaxes one and puts one to sleep. Acute administration of ethanol may decrease sleep latency, but this effect dissipates after a few nights. In addition, waking time during the latter part of the night is increased, and there is a pronounced rebound insomnia that occurs once the ethanol use is discontinued. Except as an emergency treatment to reduce uterine contractions and delay birth, the therapeutic use of oral ethanol is confined to treating poisoning from methanol and ethylene glycol. Most of ethanol's therapeutic benefits are derived from applying it to the skin, since it is an excellent skin disinfectant. Ethanol can lessen the severity of dermatitis, reduces sweating, cools the skin during a fever and, when added to ointments, helps other drugs penetrate the skin. These therapeutic uses for ethanol are for acute problems only.
Until recently, it had been felt that the chronic drinking of ethanol led only to organ damage. Recent evidence suggests that low or moderate intake of ethanol (1-2 drinks per day) can indirectly reduce the risk of heart attacks. The doses must be low enough to avoid liver damage. This beneficial effect is thought to be due to the elevation of high-density lipoprotein cholesterol (HDL-C) in the blood which, in turn, slows the development of arteriosclerosis and, presumably, heart attacks. This relationship has not been proven, but has been culled from the results of several epidemiological studies.
Several mechanisms have been proposed to explain how oral ethanol exerts its effects. One is thought to be its ability to alter the fluidity of cell membranes—particularly neurons. This disturbance alters ion channels in the membrane resulting in a reduction in the propagation of neuronal transmission. The anesthetic gases share this property with ethanol. Furthermore, it has been shown that the degree of membrane disordering is directly proportional to the drug's lipid solubility. It has also been argued that such membrane effects occur only at very high doses. More recently, scientists have reported that ethanol may augment the activity of the neurotransmitter GABA by its actions on a receptor site close to the GABA receptor. The effect of this action is to increase the movement of chloride across biological membranes. Again, this effect would alter the degree to which neuronal transmission is maintained.
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