Acute Alcohol Intake Research Articles

Immune suppression after acute ethanol ingestion and thermal injury

Acute alcohol ingestion is commonly associated with burn injury. Both alcohol ingestion and burn injury produce immune suppression, but the combination of these factors on immune function has not been investigated. To study this combined effect, immune function was measured in rats with a 30% burn injury following a single ingestion of 2.4 g/kg of ethanol (EtOH) and compared to that of animals with burn injury only, animals with EtOH only, and animals with neither alcohol nor burn injury. Four days after ethanol and/or burn, animals receiving both ethanol and burn injury had significant suppression of in vivo chemotaxis and lymphocyte responsiveness to lipopolysaccharide (LPS) compared to animals receiving either burn injury alone or EtOH alone ( P < 0.05). There was no difference in responsiveness to concanavalin A (Con A). Serum corticosterone was significantly elevated by burn injury but not EtOH ingestion. EtOH treatment prior to injury caused a further increase in corticosterone level that was significantly associated with a decrease in immune function. These results indicate that a single EtOH exposure prior to burn injury produces greater immune suppression than does burn injury alone. This further decrease in immune function may contribute to increased susceptibility to infection and increased mortality in burn patients with acute EtOH ingestion.

Serum and saliva sex hormone levels in !Kung San men

Serum concentrations of testosterone (Tser), 5 alpha-dihydrotestosterone (DHT), estradiol 17 beta (E2), and free testosterone in saliva (Tsal) were determined by means of the radioimmunoassay method in 114 !Kung San men living in the Bushmanland district of Namibia. The healthy men (mean age 26.4 years) were asked about their dietary habits over the last two months and their acute alcohol intake during the 24 hours preceding the blood and saliva sampling. Although the sex hormone status of the !Kung lies within the range of normal men reported for Caucasoid samples, both Tser and Tsal exhibit relatively low concentrations in comparison to the great majority of published mean values. On the other hand, comparatively high DHT levels point to an elevated 5 alpha-reduction of testosterone to DHT in our sample. Estradiol concentrations show no deviation from normal values reported elsewhere for healthy young men. Different dietary habits of the !Kung lead to significant differences in their sex hormone status: both levels of Tsal and the androgen ratio Tsal/Tser decrease with increasing supplement of the traditional hunter-gatherer diet with domestic and Western food products. The amount of alcohol consumed during the day before the blood and saliva sampling shows a significant effect on the DHT metabolism, and the shorter the time after drinking, the greater decrease of DHT and DHT/E2 can be observed.

Lack of effect of acute alcohol ingestion on plasma lipids

Lack of effect of acute alcohol ingestion on plasma lipids

Physical exercise after alcohol intake: effect on plasma catecholamines and lymphocytic beta-adrenergic receptors.

The combined effects of alcohol intoxication and intense physical exercise on the adrenergic system were studied in eight healthy male volunteers. Ethanol (0.8 g/kg body weight) was administered perorally to bring about a mean serum concentration of 21 mmol/liter (0.1%); each subject also participated in an identical control session without alcohol. Acute alcohol intake alone did not change the concentrations of plasma adrenaline or noradrenaline or the density, affinity, and functioning (ability to mediate catecholamine-stimulated production of cAMP) of lymphocytic beta-adrenergic receptors. In contrast, acute ergometer exercise brought about an approximately 10-fold increase of plasma adrenaline and noradrenaline concentrations, a 2- to 3-fold increase of beta-adrenergic receptor density and an enhancement of isoproterenol-stimulated cAMP production. Alcohol intake immediately before the ergometer exercise did not modify these changes. In conclusion, acute physical exercise activates the human adrenergic system, with an increase of both plasma catecholamines and lymphocytic beta-adrenergic receptors. Moderate alcohol intoxication does not affect exercise-induced alterations of these parameters.

Decreased Isotretinoin Efficacy during Acute Alcohol Intake

Decreased Isotretinoin Efficacy during Acute Alcohol Intake

Management Issues for Trauma Patients with Alcohol

An estimated 20-25% of patients treated in emergency departments or as inpatients for trauma have been drinking and most of them have BACs of 0.10 gm/dL (22 mmol/L) or higher. Many are problem drinkers or alcoholics, smokers, and also abuse other drugs. Both acute ingestion and chronic abuse of alcohol increase the frequency and severity of injury, and may complicate patient management by mimicking head trauma, masking intra-abdominal injury, causing circulatory collapse, reducing immune response, altering hepatic metabolism, or causing delirium tremens. Proper management of a trauma patient with alcohol includes BAC determination, careful history taking for alcoholism with referral for further evaluation or treatment when indicated, and determination whether other drugs are also being misused. Failure to do these may put a physician at legal risk both for improper care of the patient and for exposing others to injury if the patient crashes after being discharged from the emergency department while still impaired by alcohol.

The Pulsatile Secretion of Gonadotropins and Growth Hormone, and the Biological Activity of Luteinizing Hormone in Men Acutely Intoxicated with Ethanol

The effects of acute alcohol ingestion were studied on pulsatile secretion of immunoreactive luteinizing hormone (LH), follicle-stimulating hormone (FSH), and growth hormone (GH), and on serum bioactive LH, testosterone, cortisol, and prolactin. A dose of 1.5 g ethanol per kg of body weight was administered by mouth to eight healthy male volunteers (aged 20 to 26 years) during 3 hr from 1800 to 2100 hr. Blood samples were collected every 20 min for 20 hr until 1400 hr of the following day. Each subject served as his own control in an identical experiment without ethanol, carried out at least 1 month later. Ethanol ingestion decreased serum testosterone concentration on average by 23% (p less than 0.05) between 10 and 16 hr after starting the drinking. The mean levels of LH and FSH and the mean number and amplitude of LH and FSH pulses remained unchanged. Ethanol ingestion did not affect the biological activity of LH. In each subject alcohol administration reduced the nightly peak of GH secretion, and in addition, changed the timing of this peak in most subjects. Only marginal changes were found in the prolactin levels but ethanol ingestion increased the cortisol levels on average by 36% (p less than 0.05) between 11 and 14 hr after the start of drinking. We conclude that the decrement in serum testosterone evoked by ethanol is not attributable to impaired pulsatile secretion of gonadotropins nor to reduced biological activity of LH. In contrast, ethanol profoundly suppressed the pulsatile secretion of growth hormone.

Nifedipine-Alcohol Interaction

To the Editor.— We wish to report an interaction of oral nifedipine with acute alcohol ingestion. Study— Ten healthy, male volunteers were recruited, prescreened, and the study completed according to Canadian Medical Research Council guidelines for clinical studies. Following an overnight fast volunteers were randomized in a cross-over design to receive either a single 20-mg dose of nifedipine (two 10-mg capsules) administered with 150 mL of orange juice or nifedipine with a mixture of 75 mL of orange juice and 75 mL of 94% ethanol (0.8 g/kg). 1 Over a 16hour time period, following both regimens, pulse rate and blood pressure were monitored along with plasma nifedipine profiles, measured by gas chromatography with electron capture detection. The area under the plasma concentration-time profile of nifedipine was increased by 54% ( P

Acute Alcohol Ingestion Reduces Fatty Acid Extraction of the Heart, Liver, and Small Intestine

Ethanol may have profound effects on both the distribution of perfusion and substrate utilization by the liver and heart due to its vasodilating properties and the generation of high levels of circulating acetate and lactate. Since fatty acids are highly extracted by the heart and liver under normal circumstances, changes in the relationship of perfusion/fatty acid uptake may be a sensitive indicator of both altered perfusion and changes in metabolic substrate availability. To test this hypothesis, studies were performed in rats fed 3.1, 6.2, and 9.3 g/kg doses of ethanol. Fatty acid uptake was estimated with a 3-methyl substituted reagent with a chain length equivalent to 17 carbons. The methyl group in the three position prevented beta oxidation and prolonged the residence of fatty acids in the tissue. Eighteen hours after acute alcohol administration, fatty acid uptake was reduced in the heart and the small intestine; in the liver uptake was increased or unchanged. Acute ethanol administration also resulted in increased perfusion, as indicated by enhanced uptake of 201thallium by the heart, liver, and small intestine. The fatty acid extraction of the heart, liver, and small intestine, defined as the concentration of fatty acid divided by the concentration of 201thallium, was markedly decreased by alcohol ingestion. These alcohol effects were dose-dependent and temporally related. The data suggest that ethanol ingestion could potentially alter heart function during exercise or following a prolonged fast, when the heart relies primarily upon fatty acids extracted from the circulation to generated adenosine triphosphate (ATP).

Effects of Acute Alcohol Intake on Tolerance to Hypotension

The specific aim of this research was to test the hypothesis that intoxication with alcohol results in poor tolerance to hemorrhage. This was evaluated on the basis of blood pressure, cardiac output respiratory rate, blood flow to organs, and survival for 4 hr after hemorrhage. Four groups of six swine per group were used (control, intoxicated, hemorrhage, and intoxicated-hemorrhage). The results revealed that blood alcohol concentrations near 0.1% greatly reduced tolerance to hemorrhage. Intoxicated animals subjected to hemorrhage were unable to maintain an adequate cardiac output, blood pressure, or respiratory rate to sustain life. Pigs tolerated higher blood alcohol concentrations, up to 0.35%, when not exposed to hemorrhage. Also, unintoxicated pigs were able to compensate for severe hemorrhage. Only one of the six pigs in the intoxicated-hemorrhage group survived for 4 hr after hemorrhage. In conclusion the body's ability to compensate and recover from hemorrhage was greatly reduced during intoxication. It is logical to assume that the ability to overcome numerous other stressors may also be reduced during intoxication.

Discrimination of motion in depth trajectory following acute alcohol ingestion

Evoked potentials were recorded at four scalp sites O1, O2, T5, T6; before and after the consumption of one of two alcohol dose levels, to the occurrence of disparate stimuli in dynamic random dot stereograms. Twenty young adult subjects, all of whom had vision which was normal or corrected to normal, were randomly assigned to the two dosage groups. Subjects viewed stimuli which embodied crossed disparity and followed one of three trajectories in depth. The task was to distinguish between and identify, by specific button presses, these trajectories. One half of the stimuli were presented with monocular cues to motion in depth (dark condition); in the remainder only stereoscopic depth information was available (uniform condition). Responses to both conditions showed alcohol-related reduction of evoked responses across all sites. It was concluded that the visual systems associated with the processing of motion in depth were susceptible to alcohol effects, as revealed by reductions in the amplitude of evoked responses.

Effects of Jian Bu Wan – a traditional Chinese medication on behavioral and cardiovascular parameters after acute alcohol intake in normal subjects

The present investigation studied Jian Bu Wan's effect on «hangover», induced by acute alcohol withdrawal symptoms after a light alcohol intoxication. We found no difference between placebo of Jian Bu Wan's treatment in the effects on «hangover» symptoms

The effect of ethanol on exercise-induced muscle damage.

The effect of ethanol ingestion on exercise-induced muscle damage was examined. It has been reported that a reduced leakage of muscle proteins was found when alcohol was ingested prior to exercise. The results of that study were confounded by repeating the same exercise using the same muscle groups; the alcohol treatment was always given on the second exercise bout so that the reduced protein leakage may be due to a rapid training effect. The present study was designed to control for rapid training effect when examining the effects of ethanol ingestion on exercise-induced protein leakage from muscle. Also, this study examined the effect of acute ethanol ingestion on other indicators of muscle damage: force generation, muscle stiffness and muscle soreness. Ten women subjects performed two similar exercise regimens, one with each arm, separated by at least 10 days. Alcohol was ingested prior to exercising one arm and a nonalcoholic beverage ingested prior to exercising the contralateral arm. The exercises resulted in increased serum creatine kinase activity (p less than .05) and muscle pain (p less than .01), and decreased range of motion (p less than .01) and strength (p less than .01), indicating muscle damage. There was no significant difference between the alcohol and nonalcohol conditions for any criterion measure. It was concluded that acute ingestion of alcohol has no effect on several indicators of exercise-induced muscle damage.

Alcohol and Drug Interactions

Interactions of ethyl alcohol with various drugs are common. Their consequences vary depending on the effects of the drugs concerned, the doses of drugs and alcohol given and their mode of administration. Pharmacokinetic interactions refer to altered tissue concentrations of alcohol or drugs or both and their metabolites which sometimes lead to serious toxic reactions. The kinetic interactions take place in the absorption or metabolism of alcohol or the drug, whereas significant interactions in their distribution phase are rare. Pharmacodynamic interactions refer to the combined actions, even serious ones, which primarily take place at the tissue (receptor?) level, with or without an important pharmacokinetic component of interaction. Acute substantial doses of alcohol given quickly tend to inhibit microsomal drug metabolism and thus enhance the effects of drugs. Chronic administration of alcohol usually induces the synthesis of cytochrome P-450 isoenzyme P-450 II E1, thus accelerating the metabolism of its own and, depending on the circumstances, of various drugs as well. Reduced actions of the agents may then ensue. If the (toxic) effect of a drug (e.g., paracetamol) depends on the formation of active metabolites acute intake of alcohol may, paradoxically, reduce the drug effect, while chronic alcohol intake enhances it. Induction of hepatic enzymes by alcohol may affect the turnover of endogenous vitamins and hormones, or even produce carcinogenic substances.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of Acute Alcohol Ingestion on the Left Ventricular Performance of Normal Subjects Before and After Incomplete Autonomic Blockade

The effects of acute alcohol ingestion on the left ventricular performance of nine normal subjects, mean age 25 years, were studied before and after incomplete autonomic blockade, produced by atropine, 0.04 mg/kg body weight, and propranolol, 0.2 mg/kg body weight. Left ventricular (LV) function curves (stroke volume vs. end-diastolic volume) were plotted from data generated before and after large variations in cardiac preload. Increase in preload was produced by five degrees of head-down tilt for 90 minutes; decrease in preload was produced by graduated lower body negative pressure to -40 mmHg. After incomplete autonomic blockade, the negative inotropic effects of acute alcohol ingestion were minimal but significant and manifest by the reduction in mean velocity of circumferential fiber shortening (p less than 0.05). Studies during wide variations in preload confirmed the importance of maintaining central blood volume after alcohol ingestion. Lower body negative pressure after both incomplete autonomic blockade and alcohol produced a further deterioration in mean velocity of circumferential fiber shortening (p less than 0.05).

Effect of Acute Ethanol Intake and Hangover on the Levels of Plasma and Urinary Catecholamines and Lymphocytic β‐Adrenergic Receptors

To determine whether acute ethanol administration affects the function of the adrenergic system the concentrations of plasma catecholamines and cyclic AMP (cAMP), the level of lymphocytic beta-receptors, the concentration of basal and isoproterenol-stimulated lymphocytic cAMP and the excretion of urinary catecholamine metabolites were studied in six healthy men. These parameters were also measured during the hangover, both under resting condition and during an anaerobic ergometer exercise. Acute intake of ethanol (1.5 g/kg body weight) had no statistically significant effect either on plasma adrenaline and noradrenaline concentrations or beta-adrenergic receptor levels. Ethanol consumption did neither change the urinary excretion of catecholamine metabolites (homovanillic acid, normetanephrine, metanephrine, and 3-methoxyhydroxymandelic acid). Exercise was associated with a 6-10-fold elevation in plasma adrenaline and noradrenaline concentrations and with a two- to threefold elevation on beta-adrenergic receptor levels. This effect of exercise was not modified by preceding alcohol intake and resulting hangover. These preliminary findings suggest that acute alcohol intake does not significantly alter the concentration and functioning of human beta-adrenergic receptors.

EFFECT OF ACUTE ETHANOL INGESTION ON HUMAN GASTRIC LUMINAL PROSTAGLANDIN E 2 , PROSTAGLANDIN F 2α AND 6-KETO-PROSTAGLANDIN F 1α

In healthy human volunteers we evaluated the effect of a single oral dose of 1 g/kg of alcohol (12.5%, v/v) on the output of prostaglandin E2, prostaglandin F2 alpha and 6-keto-prostaglandin F1 alpha in the gastric juice. In control experiments performed at intervals of 5-8 days, the subjects received the identical volume of water. Ninety minutes after the ingestion of alcohol, or water, first the basal secretion and subsequently the secretion after injection of pentagastrin (6 micrograms/kg, i.m.) were collected over periods of 60 min. The concentrations of the three prostaglandins were determined by radio-immunoassay. After ingestion of alcohol, the volume of gastric juice in response to pentagastrin stimulation was reduced by 24.6%, as compared with the control period. Ingestion of alcohol led to a significant reduction in the concentration of prostaglandin E2 (-42.7%) after stimulation with pentagastrin. The prostaglandin E2 output per hour was markedly inhibited by the ingestion of alcohol, both in the basal period (-47%) and after stimulation with pentagastrin (-55%). While stimulation with pentagastrin did not influence the secretion of PGE2 or PGF2 alpha, the output of 6-keto-PGF1 alpha increased appreciably (+88%) after the administration of pentagastrin. Alcohol also significantly (-28%) inhibited the secretion of 6-keto-PGF1 alpha in the period following the administration of pentagastrin. It is supposed that the inhibition of the secretion of prostaglandin E2 and 6-keto-prostaglandin F1 alpha by acute alcohol ingestion, might be of significance for the development of alcohol-induced mucosal damage in the stomach.

Effect of acute and chronic alcohol feeding on prostaglandin E2 biosynthesis in rat stomach.

The effect of acute and chronic alcohol ingestion on gastric prostaglandin E2 synthesis and the PGE2 content in the stomach was studied in rats. Up to 8 hr following a single oral load of 20% alcohol (v/v; 4 g/kg body weight), the PGE2 synthesis in isolated microsomes from rat stomach remained unchanged as compared with control values. Feeding a liquid alcohol-containing diet (37% of total Joules) for 1, 6, or 12 weeks significantly decreased the rate of PGE2 synthesis (percentage inhibition as compared with control values 39, 27, and 57, respectively). In addition, chronic alcohol feeding led to a drop in the tissue content of PGE2, the decrease being more pronounced after 6 (-49%) and 12 (-58%) weeks than after 1 week (-24%). The results suggest that the inhibition of endogenous PGE2 synthesis in the stomach following ingestion of appreciable quantities of alcohol might play a role in the pathogenesis of alcohol-induced injury of the gastric mucosa.

Alcohol Effects on Naltrexone-Induced Stimulation of Pituitary, Adrenal, and Gonadal Hormones During the Early Follicular Phase of the Menstrual Cycle*

Chronic alcohol abuse in women is associated with severe derangements of menstrual cycle regularity. However, acute alcohol ingestion has no effect on pituitary-gonadal secretory function. The purpose of this study was to determine whether acute alcohol ingestion altered the effects of naltrexone, a long-acting opioid antagonist, on pituitary, adrenal, and gonadal hormones in normal women. Fourteen women were studied during the early follicular phase (between days 2 and 4) of their menstrual cycle. Plasma LH, PRL, estradiol, progesterone, and cortisol concentrations were measured before and after administration of 50 mg naltrexone, orally, and alcohol or placebo solution given 1 h after naltrexone, under double blind conditions. Naltrexone significantly increased mean plasma LH (P = 0.02), PRL (P = 0.003), E2 (P less than 0.03), and cortisol (P less than 0.001) levels. Alcohol significantly augmented the naltrexone-stimulated increases in plasma LH (P = 0.006), estradiol (P less than 0.004), and cortisol (P less than 0.001) levels and significantly decreased plasma progesterone levels (P = 0.001). Plasma PRL increased (P = 0.001) to the same extent after naltrexone and alcohol ingestion or naltrexone and placebo. We conclude that alcohol enhances naltrexone-induced increases in plasma gonadotropins and adrenal and gonadal steroid hormones in women during the early follicular phase of the menstrual cycle.

Hypoploidy and hyperplasia in the developing brain exposed to alcohol in utero.

Prenatal effects of acute maternal alcohol ingestion on chromosome segregation and mitotic frequency in the brain cells of the fetus were evaluated in mice by direct chromosome and mitotic counts and by flow cytometry. Fetuses were exposed to acute transplacental doses of alcohol for 4 days and killed on the fifth day. Those litters in which the fetuses were developed to the equivalent of normal 16th-17th-day gestation age were analyzed. A marked increase in the number of hypoploid metaphases was observed in direct proportion to the dose ingested by the mother. An over 30% increase in hypoploidy over controls was measured in the fetuses exposed to the highest dose. Counts of mitotic cells showed an over tenfold increase in the mitotic index of the fetal brain exposed to alcohol. Flow cytometric measurements of DNA content in isolated fetal brain cell nuclei showed a shift from a single G0/G1 peak in controls to a bimodal G0/G1-G2 + M distribution in alcohol-exposed fetuses of the same developmental age.