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Biomedical subjects

J Neiman

Publications and source records attributed to J Neiman.

At least 19 recordsLinked to original sources
PubMed1991

Late auditory evoked potentials in alcoholics. Identifying those with a history of epileptic seizures during withdrawal.

The N1-P2 wave of the auditory evoked potential was studied in 19 alcoholics, six of whom had withdrawal seizures on previous admissions. The recordings were made at 1 and 5 days after cessation of drinking. Eight nonalcoholic volunteers were used as controls. The latencies of N1 and P2 were slightly prolonged in alcoholics, but during the detoxification period they frequently shortened (p less than 0.05), occasionally attaining the values of the controls. One day after withdrawal, the amplitude of N1-P2 was consistently reduced in the alcoholics compared to the controls (p less than 0.05 and p less than 0.01), but higher in alcoholics with a seizure history compared to alcoholics without seizures (p less than 0.05 and p less than 0.001). Five days after cessation of drinking, the amplitude in the alcoholic groups always increased from the admission values (p less than 0.05 and p less than 0.01). By that time, the alcoholics with a history of withdrawal seizures had significantly (p less than 0.05 and p less than 0.01) higher amplitudes than those of the controls or the alcoholics without seizures. Large N1-P2 amplitude during alcohol withdrawal may reflect increased cerebral excitability and contribute to the identification of alcoholics with high risk for withdrawal seizures.

Adult↗
PubMed1990

Effects of alcohol withdrawal on responses of platelets from alcoholics--a study using platelet-rich plasma from blood anticoagulated with D-phenylalanyl-L-prolyl-L-arginyl chloromethyl ketone (FPRCH2Cl).

Platelet responses stimulated by a range of concentrations of ADP or collagen were studied in platelet-rich plasma (PRP) from alcoholics 24-36 h and 6 days after cessation of drinking, and in PRP from age- and sex-matched controls. The studies were done using plasma from blood anticoagulated with the specific thrombin inhibitor D-phenylalanyl-L-prolyl-L-arginyl chloromethyl ketone (FPRCH2Cl, PPACK); the use of this compound permits the study of platelet responses in plasma at physiological concentrations of ionized calcium. Responses of platelets to ADP (primary aggregation) and collagen (aggregation, secretion of [14C]serotonin from prelabelled platelets, and thromboxane formation) were lower in alcoholics 24-36 h after withdrawal of alcohol compared with controls. This inhibition of platelet function was not due to the presence of alcohol in the blood of the alcoholics. Aggregation in response to ADP did not change during the withdrawal period studied, while collagen-induced aggregation and secretion increased significantly and collagen-induced thromboxane formation tended to increase towards control values. The reduced platelet responses observed in alcoholics and the different rates of "recovery" of different pathways of aggregation towards control values must be due to alterations either in the platelets themselves and/or in the plasma brought about by the chronic presence of ethanol, and its withdrawal.

Adult↗
PubMed1990

Late auditory evoked potentials: a method for monitoring drug effects on the central nervous system.

An auditory event-related potential paradigm was designed to objectively quantify the effects of drugs on the central nervous system (CNS). A series of tones was presented at three random interstimulus intervals (ISI). The amplitude of N1-P2 and the recovery of this complex across ISI appear to be rapid, reliable and sensitive measures of changes in brain function associated with drug intake. To illustrate, an acute dose of diazepam was administered orally to a small group of normal subjects. The amplitude of N1-P2 was reduced and the slope of recovery flattened, indicating a decrease in CNS excitability concomitantly with the established pharmacokinetics of the drug.

Acoustic Stimulation↗
PubMed1990

Movement disorders in alcoholism: a review.

A wide variety of movement disorders are associated with alcohol abuse. Some idiopathic movement disorders are markedly improved by small amounts of alcohol and this response occasionally may lead to alcoholism. Alcohol abuse alone or combined with hepatic encephalopathy can cause various types of tremor, asterixis, and cerebellar dysfunction. Alcohol withdrawal is occasionally complicated by transient basal ganglia dysfunction manifested by parkinsonism or chorea. These syndromes are distinct from the movement disorders complicating acquired hepatolenticular degeneration occurring in some chronic alcoholics. This review discusses the clinical and pathophysiologic aspects of the movement disorder syndromes that complicate alcohol abuse.

Alcoholism↗
PubMed1989

Platelet responses to platelet-activating factor are inhibited in alcoholics undergoing alcohol withdrawal.

Platelet aggregation, secretion of serotonin, and formation of thromboxane B2 induced by platelet-activating factor (1-O-alkyl-2-acetyl-sn-glyceryl-3-phosphorylcholine) were studied in plasma containing physiological concentrations of ionized calcium in eight alcoholics after cessation of heavy drinking. Responses of platelets of four nonalcoholic volunteers, matched with a subgroup of the alcoholics by age and sex, were also investigated. Aggregation of platelets from alcoholics was significantly less throughout the 6-day detoxification period compared with controls. Secretion of serotonin (5-hydroxy-tryptamine) was negligible and the production of thromboxane B2 was not detectable. Decreased platelet aggregability in response to aggregating agents, including platelet-activating factor, may be important in the development of hemorrhagic complications in alcoholics.

Adult↗
PubMed1988

Effects of ethanol on platelet thromboxane formation after ethanol withdrawal in chronic alcoholics: an in vitro study.

The effect of ethanol on the formation of platelet thromboxane B2 (TXB2), a stable metabolite of thromboxane A2 (TXA2) was studied in vitro in six chronic alcoholics, admitted for detoxification, and in six healthy volunteers. Immediately after cessation of heavy drinking platelet count and ADP-induced TXB2 formation were lower in alcoholics than in nonalcoholic volunteers (P less than 0.05). Ten days after withdrawal of ethanol platelet count increased, and skin bleeding time shortened (P less than 0.05). Ethanol had no effect on arachidonate-induced platelet TXB2 formation, whereas ethanol added to platelet suspension prior to stimulation by ADP resulted in a concentration-related inhibitory tendency in both alcoholics and nonalcoholic control subjects. This effect of ethanol may be of significance for primary hemostasis in alcoholics.

Adenosine Diphosphate↗
PubMed1988

Concentration-time profiles of ethanol and acetaldehyde in human volunteers treated with the alcohol-sensitizing drug, calcium carbimide.

1. The disposition kinetics of ethanol and its toxic metabolite acetaldehyde were investigated in 10 healthy male volunteers who ingested 0.25 g kg-1 ethanol after an overnight fast. This dose of ethanol was given 2 h after they swallowed a tablet of either calcium carbimide CC (50 mg), a potent inhibitor of low Km aldehyde dehydrogenase (ALDH), or placebo according to a single-blind crossover design. 2. The pulmonary blood concentrations of ethanol and acetaldehyde were estimated indirectly by means of a gas chromatographic method modified for analysis of end-expired breath. This non-invasive sampling technique allowed replicate determinations at 15 min intervals. 3. The distribution volume of ethanol (V) was 0.64 +/- 0.023 1 kg-1 after CC and 0.68 +/- 0.026 l kg-1 after placebo treatment (P greater than 0.05). The zero order slope of the blood-ethanol decay profile (ko) decreased by about 5% when low Km ALDH was inhibited. The elimination of ethanol from the body (V X ko) was 1.9 +/- 0.051 mmol kg-1 h-1 after CC compared with 2.11 +/- 0.056 mmol kg-1 h-1 in placebo control experiments (P less than 0.001). The area under the ethanol concentration time curve (0----180 min) increased after CC treatment implying a change in clearance. 4. The disposition of acetaldehyde was markedly different in subjects pretreated with CC. The peak blood-concentrations, estimated by analysis of breath, ranged from 40-242 mumol l-1 compared with 1.7-6.5 mumol l-1 after placebo.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetaldehyde↗
PubMed1988

Platelet thromboxane formation capacity after ethanol withdrawal in chronic alcoholics.

Collagen-, arachidonate- and ADP-stimulated platelet thromboxane B2 (TXB2) formation was studied in platelet-rich plasma (PRP) of 14 alcoholics, 7 of whom had a biopsy-verified alcoholic fatty liver. On admission for detoxication, the alcoholics showed decreased platelet count and aggregability (p less than 0.001) as compared to nonalcoholic healthy controls. Platelet TXB2 formation was decreased (p less than 0.01), if PRP was stimulated by arachidonate, but not if it was stimulated by ADP or collagen. In contrast, 9-14 days after ethanol withdrawal platelet TXB2 formation had increased to markedly higher levels than those seen in nonalcoholic controls (p less than 0.01), if PRP was stimulated by ADP, but not if it was stimulated by arachidonate or collagen. Skin bleeding time was found to be prolonged (p less than 0.05) on admission in alcoholics having fatty liver, but it normalized within 2 weeks after ethanol withdrawal. We conclude that the effect of ethanol withdrawal in alcoholics on platelet TXB2 formation is influenced by platelet count, aggregability and the agonist used to induce platelet aggregation.

Adenosine Diphosphate↗
PubMed1987

Platelet uptake of serotonin (5-HT) during ethanol withdrawal in male alcoholics.

Changes in the kinetic variables of the platelet serotonin uptake, Km and Vmax, were studied in 7 male alcoholics, admitted for detoxification and in sex- and age-matched volunteers. On admission the alcoholics had lower Km values than reference subjects (p less than 0.05). During detoxification the Km values normalized. Vmax was normal throughout the study in spite of the changes in platelet count. The results of the study suggest that the affinity of serotonin to its uptake receptor is transiently increased after a period of heavy drinking.

Adult↗
PubMed1987

Composition of platelet phosphatidylinositol and phosphatidylcholine after ethanol withdrawal.

Platelet phosphatidylinositol and phosphatidylcholine composition, ADP-induced platelet aggregation and associated thromboxane B2 formation were studied in alcoholics after a period of heavy drinking and in healthy non-alcoholic volunteers. The composition of these phospholipids in alcoholics was different from that seen in the control subjects. The most prominent change was a decrease in the relative amount of stearoyl-arachidonoyl species in the phosphatidylinositol fraction. Particularly this species of PI might be involved in the transmission of transmembrane signals. During detoxification changes were also observed in the extent of ADP-induced platelet aggregation and the amount of thromboxane B2 produced. Changes in platelet phospholipid composition might influence platelet reactivity in alcoholics.

Adenosine Diphosphate↗
PubMed1987

Effects of vitamin E therapy on ethanol-induced changes in platelet aggregation, thromboxane formation, factor VIII levels and serum lipids.

A transient increase in platelet thromboxane formation has been observed in non-alcoholics during acute ethanol intoxication and in alcoholics shortly after ethanol withdrawal. Whether these effects are related to the generation of free radicals and lipid peroxidation was investigated by using vitamin E as a free radical scavenger and inhibitor of lipid peroxide formation. The results demonstrate that a high dose of vitamin E (1800 IU) taken daily by non-alcoholic men slightly (P less than 0.05) decreases aggregation-associated platelet thromboxane formation during ethanol oxidation. Likewise, vitamin E prevents the ethanol-induced increase (P less than 0.01) in factor VIII coagulant activity. These observations suggest that the enhancement of platelet thromboxane formation and factor VIII coagulant activity by acute ethanol ingestion may be related to stimulated lipid peroxidation. By contrast, similar effects of vitamin E were not found in alcoholics shortly after ethanol withdrawal suggesting other mechanisms for their platelet hyperreactivity.

Adult↗
PubMed1987

Urinary excretion of 2, 3-dinor-6-keto prostaglandin F1 alpha and platelet thromboxane formation during ethanol withdrawal in alcoholics.

The excretion of 2,3-dinor-6-keto prostaglandin F1 alpha, a major urinary metabolite of prostacyclin, and the formation of thromboxane B2, a stable metabolite of thromboxane A2, by platelets stimulated by adenosine diphosphate, were studied in alcoholics, who had been admitted for detoxification. Once prolonged heavy drinking had stopped, platelet count and thromboxane formation, calculated either per 10(7) platelets or per litre of blood, significantly increased (p less than 0.05), while the skin bleeding time and urinary excretion of the metabolite of prostacyclin decreased (p less than 0.05). The balance between prostacyclin and thromboxane therefore seemed to favour the excretion of prostacyclin while it shifted to favour thromboxane formation about a week later.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Effects of a small dose of ethanol and calcium carbimide-induced acetaldehyde intoxication on human platelet aggregation, associated thromboxane formation and urinary excretion of 2,3-dinor-6-keto prostaglandin F1 alpha.

We studied ADP-induced platelet aggregation, associated thromboxane B2 (TXB2) formation, urinary excretion of the prostacyclin metabolite 2,3-dinor-6-keto prostaglandin F1 alpha (2,3-dinor-6-keto PGF1 alpha) and formation of malondialdehyde in 10 healthy volunteers after ingestion of a small dose of ethanol (0.25 g per kg of body weight) and calcium carbimide (50 mg). Platelet aggregation in platelet-rich plasma (PRP) was suppressed (p less than 0.05) by ethanol, but no change occurred in platelet TXB2 formation. Ingestion of calcium carbimide caused significant elevations in blood acetaldehyde (p less than 0.001) and ethanol (p less than 0.05) levels, but acetaldehyde did not influence platelet aggregability or the aggregation-associated TXB2 formation. However, calcium carbimide per se significantly (p less than 0.05) elevated TXB2 formation. No effects were found on plasma malondialdehyde levels and urinary excretion of 2,3-dinor-6-keto PGF1 alpha. These observations indicate that a small dose of ethanol attenuates platelet aggregation without any significant effect on aggregation-associated TXB2 formation. By contrast, ingestion of calcium carbimide per se may enhance TXB2 formation.

6-Ketoprostaglandin F1 alpha↗