[Acetaldehyde and some biochemical parameters in alcoholic intoxications]. / Atsetal'degid i nekotorye biokhimicheskie parametry pri alkogol'nykh intoksikatsiiakh.

The need in comprehensive gas chromatography and biochemistry examinations is grounded for cadaver expertise in order to cope with issues related with alcoholic intoxication. Descriptions of 3 examination methods of biological fluids are elucidated, i.e. gas chromatography, electrophoresis and fixing of a degree of endogenous intoxication. The concentration of acetaldehyde in 3 body media (blood, urine and liquor) are analyzed in detail; the isoenzyme spectra of lactate-, alcohol- and aldehyde dehydrogenase as well as the contents of medium molecules in death of alcohol poisonings and due to mechanical trauma are also in the focus of attention.

[The diagnostic value of determining the level of acetaldehyde in blood, urine, and cerebrospinal fluid]. / Diagnosticheskoe znachenie opredeleniia atsetal'degida v krovi, moche i likvore.

The contents of acetaldehyde (AA) in biological fluids obtained from the dead with the confirmed lethality causes, i.e. ischemic heart disease (IHD), alcoholic cardiomyopathy (ACMP) and mechanical traumas (MT), were examined on an actual forensic-medical material (AFMM). 14 death cases of males, aged 18 to 45, were studied. The method of gas-liquid chromatography (GLC), or rather its variation of vaporphase analysis, was used to state the presence and to assess the concentration of acetaldehyde. The results revealed differences between concentrations of acetaldehyde in the examined groups depending on the presence or absence of alcoholemia. Thus, the AA concentrations were found in trace quantities in the MT group free of alcoholic intoxication; while, when it was present in this group, the concentrations went up several-fold. A higher AA content was typical of the ACMP group in all examined subjects both with and without alcoholic intoxication. The final study results are suggestive of that the AA determination in blood, urine and liquor by GLC could be used, within the forensic medical practice, in assessing a severity degree of alcoholic intoxication while establishing the lethal outcome cause due to chronic pathologies and MT.

The calcium carbimide-ethanol interaction: lack of relation between electroencephalographic response and cerebrospinal fluid acetaldehyde.

Penetration of acetaldehyde into cerebrospinal fluid (CSF) was studied in healthy human volunteers during calcium carbimide-ethanol interaction. CSF was sampled via lumbar puncture and blood from a cubital vein. CSF and blood acetaldehyde concentrations varied from 1 to 41 and from 22 to 138 mumol/l, respectively. The results indicate that acetaldehyde penetrates the human blood-liquor barrier. Computer analysis of electroencephalograms (EEGs) recorded during the interaction showed reduction in alpha activity with a concomitant increase in delta activity. The changes were similar to those previously observed during 'normal' ethanol intoxication.

Acetaldehyde penetrates the blood-liquor barrier of goats.

Goats received ethanol or acetaldehyde via carotid arterial infusions. Cerebrospinal fluid (CSF) was sampled for a lateral cerebral ventricle and blood from a jugular vein. Ethanol infusions produced only negligible levels of acetaldehyde in blood and CSF, but acetaldehyde infusions resulted in high levels. In contrast to ethanol, acetaldehyde was rapidly eliminated from both blood and CSF after discontinuing the infusion. The results indicate that even small amounts of acetaldehyde easily penetrate the blood-liquor barrier of goats.

Low acetaldehyde levels in blood, breath and cerebrospinal fluid of intoxicated humans as assayed by improved methods.

A sensitive method for determination of human blood acetaldehyde (AcH), which avoids artefactual ethanol-derived Ach formation, was developed. AcH was trapped by collecting blood directly into isotonic semicarbazide, the plasma separated, AcH liberated by perchloric acid and analyzed by gas chromatography. Breath AcH was also trapped in semicarbazide and analyzed similarly. Using an experimentally determined blood:breath partition ratio of 190, calculated pulmonary blood and measured antecubital blood AcH were very similar at various concentrations. Blood AcH was found generally to be very low (< 10 microM) at moderate ethanol levels. Calcium carbimide (0.25 mg/kg) caused moderate flushing reactions and elevated AcH to 25-188 microM. 4-Methylpyrazole (5 mg/kg i.v.) rapidly attenuated AcH levels and symptoms, indicating its potential use in the treatment of disulfiram-ethanol reactions. AcH in the cerebrospinal fluid of 5 highly intoxicated patients was almost absent (0-5 microM). Blood AcH in occasional or chronic alcohol abusers were generally low (< 10 microM), elevated AcH levels being observed only in association with clinical abnormalities. The results indicate that in general, previously reported human blood AcH levels are erroneously high and that breath levels reflect blood levels. Blood AcH may play a lesser role in the actions of ethanol in humans than is often assumed.

Acetaldehyde in cerebrospinal fluid: its near-absence in ethanol-intoxicated alcoholics.

The cerebrospinal fluid of five ethanol-intoxicated alcoholics was found to contain only barely detectable (0--5 microM) concentrations of acetaldehyde, thus questioning its frequently advocated contribution to intoxication, dependence and other central ethanol effects.