[Transitory intoxicated delusions of alcoholic origin. 1906].
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The in vitro effects of some cholinergics and an anticholinergic agent on hepatic liver alcohol and aldehyde-dehydrogenase were investigated. Physostigmine was the only cholinomimetic agent which significantly inhibited hepatic mitochondrial aldehyde-dehydrogenase without concomitant changes in specific activity of alcohol dehydrogenase. This inhibitory action of physostigmine is found to be competitive and is confined to the enzyme with the low Km value which is also known to be inhibited by disulfiram. Kinetic studies were made to determine changes in the apparent Km value of aldehyde dehydrogenase by physostigmine. Additional experiments were performed to evaluate the Ki50 of physostigmine. The results are discussed in relevance to possible physostigmine-ethanol interaction and the complication of physostigmine in post-operative recovery procedures in individuals with alcohol intoxication and/or in alcoholic patients.
Six healthy men, aged 23 to 30 years, were studied by radionuclide angiocardiography at rest and at 2 submaximal exercise levels in the upright position during increasing alcohol intoxication. At light intoxication (serum ethanol 23 mmol/liter), the median value of left ventricular (LV) ejection fraction (EF) at rest decreased by 5%. At heavy intoxication (serum ethanol 45 mmol/liter), the median LVEF decreased at rest by 11% and during 75% submaximal exercise by 6%, heart rate at rest increased (median 81 vs 62 beats/min), and systolic blood pressure decreased during 50% submaximal exercise (median 145 vs 163 mm Hg). No significant changes of plasma epinephrine concentrations were recorded, whereas plasma norepinephrine concentrations were increased by 24% at rest during light intoxication and by 30 to 38% during heavy intoxication. No changes of LVEF and plasma catecholamine levels were recorded after ingestion of isovolumic, isocaloric drinks as compared with values obtained before intake. Thus, influences of ingestion per se and repeated investigations of LV function were excluded. These findings suggest that in healthy subjects alcohol intoxication causes a dose-dependent impairment of cardiac contractility. Compensatory mechanisms may account for a reduced influence during exercise.
Acute alcohol intoxication has been shown to increase physical aggression in the laboratory as measured by the Taylor aggression paradigm with independent groups. Because it would be advantageous to use the Taylor paradigm in a repeated measures design to examine individual differences, the present study compared the performance of subjects on two counterbalanced occasions: when they were intoxicated and when they were sober. Order of testing significantly interacted with drug condition for the aggression measures and pain threshold. However, an analysis of the ratio of pain threshold to shock intensity, and to total aggression, revealed the procedure to be useful in understanding one aspect of how alcohol modulates aggression. The results suggest that acute alcohol intoxication interferes with the ability to integrate previously acquired knowledge in the formulation of behavioral strategies.
This study investigated the temporal distribution of risky behaviors among injured motorcyclists, that is, riding unhelmeted or while intoxicated, and showed how they are associated with risk of fatal injuries. Data of motorcyclists injured in Khon Kaen municipality in northeastern Thailand and transferred to Khon Kaen Regional Hospital were obtained from the trauma registry system of the hospital. Case fatalities were compared by time of day, age group, helmet use, and alcohol intoxication. Unhelmeted riding peaked late in the evening and riding while intoxicated peaked around midnight. Both were associated with increased fatality risk after stratification by time of day; the odds ratios were 3.49 (95% confidence interval (CI) = 1.48-9.36) and 3.01 (CI = 1.71-5.19), respectively. Nighttime injuries were not significantly associated with increased fatality risk after stratification by helmet use or alcohol intoxication. Unhelmeted driving was prevalent and associated with higher fatality risk among younger drivers, whereas intoxicated driving was less prevalent among teens but associated with increased risk among those aged 20-39 years. This study shows that riding unhelmeted or while intoxicated can explain the increased fatality risk at night, suggesting that safety education or enforcements should be targeted at specific age groups and appropriate times.
Event-related potentials and visuospatial learning performance were examined to understand the effects of chronic alcohol use on complex information processing. A total of 18 alcoholic male in-patients in an alcohol treatment program served as participants. Nine persons were seen at time of admission to the program while intoxicated (mean BAC = 18.0 mg/dl). The second group of nine persons was seen detoxified after 4 weeks in the treatment program. Learning consisted of a paired-associate paradigm requiring participants to learn the distinct spatial positions of six, randomly presented "nonsense" shapes. The visuospatial learning performance of the intoxicated alcoholics was superior to that of the detoxified alcoholics. Evaluation of event-related potentials during the visuospatial learning task indicated that while both groups displayed greater right hemisphere amplitudes of P3, P2, N1, and N2-P3 components, the amplitudes of the latter three components were significantly greater in the intoxicated alcoholics. The overall results suggest that compared to the intoxicated alcoholic, the detoxified alcoholic may suffer a disruption in attentional mechanisms related to visuospatial information processing, providing support for a theory that alcohol ingestion serves to balance information processing in the chronic alcoholic.
Alcohol intoxication induced in the rat brain significant decrease in the monophosphoinositides level, but the di- and triphosphoinositides quantity did not change; the content of all the three studied fractions of the inositol-containing phospholipids in the liver decreased. The tendency to retain the normal level of di- and triphosphoinositides in the brain following alcohol intoxication may be considered as an important factor providing physiological condition of the brain metabolism.
Spinal epidural haematomas (sEDH) can be regarded as rare events, in principle a spontaneous and a traumatic aetiology can be distinguished. Spontaneous spinal epidural haematomas can arise, e.g. from vascular malformations, coagulopathies, etc. On the other hand, traumatic sEDH are related to, e.g. spinal trauma or intraoperative vascular injuries. With regard to clinical significance, spinal epidural haematomas accompanied by transient mild neurological symptoms up to lethal outcomes have been observed. We report on a 53-year-old male alcoholic who was found in the kitchen of his asylum in a grotesquely fixed body position, with his head and cervical spine in a maximum anteflected position. A general practitioner had ruled for a non-natural manner of death due to "broken neck" and alcohol intoxication, therefore, the prosecution authorities called for a medicolegal autopsy. At autopsy, paravertebral soft tissue haemorrhage in between the shoulder blades was disclosed. Furthermore, a spinal epidural haematoma, extending from the foramen magnum down to the middle portion of the thoracic spine was found. No fractures of vertebrae nor lesions of spine ligaments or bleedings of intervertebral discs were found. Blood alcohol concentration was determined 1.92 g/l and urine alcohol concentration was 1.76 g/l. Further morphological findings were cerebral oedema and cardiac hypertrophy; the urinary bladder was found filled to bursting. Neuropathological investigations confirmed the presence of the spinal epidural haematoma and assigned lethal significance to this finding. There were no histological signs of axonal injury. Reconstruction revealed that when sitting on a chair in a drunk condition, the individual's upper part of the body had fallen backwards in the corner and subsequently got stuck with maximum anteflection of the head and cervical spine, causing rupture of vessels and spinal epidural haematoma. Acute respiratory failure caused by impairment of the phrenic nerve following spinal epidural haematoma with potential synergism of alcohol intoxication was ascertained as the cause of death.
Central and peripheral haemodynamic changes 1 and 8 hours after alcohol ingestion were studied in seven healthy men, aged 21-30 years, by radionuclide cardiography and strain gauge plethysmography. Heart rate (HR) increased by 12% and cardiac output (CO) by 24% 1 hour after alcohol ingestion (mean serum ethanol 35 mmol/l). Left ventricular (LV) ejection fraction (EF) decreased by 5% because of endsystolic dilation and the forearm blood flow increased by 140%. Eight hours after alcohol ingestion (serum ethanol 21 mmol/l.) hangover symptoms were present in all subjects. HR and CO remained increased by 19% and 23%, respectively. A 4% increase was recorded in LVEF. The total peripheral resistance was reduced by 25%, while the forearm blood flow had returned to baseline values. No significant changes in plasma catecholamines were recorded. Apart from a slight increase in CO at 1 hour no haemodynamic changes were recorded after ingestion of an isovolumic, isocaloric drink. The present findings suggest that acute alcohol intoxication causes impairment of LV contractility, but that tachycardia results in an increase in cardiac output accompanied by an increased blood flow in the forearm. In the early hangover phase, when the serum ethanol is still elevated, cardiac output remains enhanced because of tachycardia, although the sympathetic nervous activity as measured by the plasma norepinephrine level is not influenced. A reduced total peripheral resistance may contribute to the increase in LV contractility in spite of sustained alcohol intoxication.
The influence of the new anti-alcohol drug Inmecarb on the alcohol consumption as well as on activity of the liver cytochrome P-450 system was studied in rats during chronic alcohol intoxication in the free choice situation between water and 15% ethanol solution. It was shown that voluntary alcohol consumption of different duration (10 days to 8 months) does not change the activity of liver cytochrome P-450 system. Inmecarb treatment (40 mg/kg, i.p. twice a day) during 14 days resulted in decrease of alcohol consumption in rats. This effect was most pronounced in late stages of experimental alcoholism. Inmecarb decreases the cytochrome P-450 content and suppresses the activity of aniline hydroxylase in rats with different duration of voluntary alcohol intoxication, but most pronounced effect was observed during the late stages of experimental alcoholism.