A color test for methanol.
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Colorimetry↗
Biomedical subjects
H G Giles
Publications and source records attributed to H G Giles.
Alcohol and deaths in police custody.
We examined the involvement of alcohol consumption, chronic alcohol abuse or dependence, the soundness of the police determination of alcohol-related intoxication, and the importance of other drugs in deaths in police custody in a survey of the cases reported to the Chief Coroner of Ontario during the past 10 years. The data suggest no mismanagement by the police. At least 86% of the fatalities were associated with recent alcohol consumption or chronic alcohol abuse/dependence. Use of drugs other than alcohol was far less common. Promoting use and further development of simple tests to estimate blood alcohol concentration, chronic alcohol problems, and suicide risk, before incarceration takes place, may save lives.
Adult↗
The influence of cyclosporine on abstinence from alcohol in transplant patients.
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Acetaldehyde↗
Noninvasive estimation of blood alcohol concentrations by eye vapor analysis using an electrochemical fuel cell detector.
A widely used breath analysis instrument was adapted for the noninvasive determination of blood alcohol in small animals. The instrument's response to ethanol in vapor above the lacrimal fluid was analyzed subsequent to taking vapor samples from a small eye cup for 15 sec. After ethanol administration (1.5 g/kg, orally) to rats, eye vapor measurements and venous blood samples were obtained over 5 hr. Eye vapor measurements were transposed into blood alcohol concentrations and compared with concentrations obtained by gas chromatographic analysis of blood. The correlation of concentrations obtained by the two methods yielded correlation coefficients of 0.93 and 0.95 depending on the calculation used. Eye vapor response and blood alcohol concentration were also found to be highly correlated (r = 0.96) after alcohol administration to mice and sampling for 2.5 hr after ethanol administration. Kinetic profiles obtained by eye vapor analysis and gas chromatography are virtually identical. The method described allows widespread use of a new, noninvasive approach to alcohol analysis in laboratory animals.
Alcoholic Intoxication↗
Noninvasive estimation of blood alcohol concentrations: ethanol vapor above the eye.
The present study describes, in animals, a novel approach to the in vivo, noninvasive determination of alcohol in the body. The concentration of ethanol in vapor above the lacrimal fluid in the eye was analyzed in situ by the use of a fast (1-min) gas sensor method developed previously for biological liquids. After an oral dose of 1 g/kg to 11 animals, eye vapor measurements and blood samples were obtained over 4 hr. The correlation of 61 blood ethanol concentrations obtained by the two methods yielded a correlation coefficient of 0.92 and a slope of 0.99. The metabolic rates of ethanol determined by gas chromatographic analysis of blood and by ethanol eye vapor analysis are virtually identical. The data suggest that ethanol eye vapor analysis may be an attractive, noninvasive method for the determination of ethanol in animals. The method is not subject to false high readings due to alcohol in the buccal cavity and thus might constitute an alternative to breath analysis in the human. In a separate series, ethanol was determined by head space gas chromatography in samples of blood and lacrimal fluid while the animals were under ketamine anesthesia. The correlation of ethanol concentrations in blood and lacrimal fluid (r = 0.99) shows that ethanol is distributed in lacrimal fluid which comprises part of total body water.
Animals↗
Ethanol-induced increase in portal blood flow: role of adenosine.
The mechanism by which ethanol induces an increase in portal vein blood flow was studied in rats using radiolabeled microspheres. Ethanol (2 g/kg) by gavage resulted in an increase of 50-70% in portal vein blood flow. The ethanol-induced increase in portal blood flow was suppressed by the adenosine receptor blocker 8-phenyltheophylline [ethanol, 61.8 +/- 4.1 ml.kg-1.min-1; ethanol + 8-phenyltheophylline (0.2 mg.kg-1.min-1), 44.2 +/- 2.0 ml.kg-1.min-1; P less than 0.05]. By itself, 8-phenyltheophylline (0.2 mg.kg-1.min-1) was without effect on cardiac output or portal blood flow. Adenosine infusion resulted in a dose-dependent increase in portal blood flow with a maximal effect at a dose of 0.17 mg.kg-1.min-1 (control, 41.3 +/- 2.3; adenosine, 81.7 +/- 8.0 ml.kg-1.min-1; P less than 0.05). This adenosine-induced increase in portal blood flow was inhibited by 8-phenyltheophylline in a dose-dependent manner [adenosine, 81.7 +/- 8.0 ml.kg-1.min-1; adenosine + 8-phenyltheophylline (0.2 mg.kg-1.min-1), 49.8 +/- 6.6 ml.kg-1.min; P less than 0.05]. Both alcohol and adenosine significantly reduced preportal vascular resistance by 40% (P less than 0.02) and 60% (P less than 0.01), respectively. These effects were fully suppressed by 8-phenyltheophylline. It is concluded that adenosine is a likely candidate to mediate the ethanol-induced increase in portal vein blood flow. It is suggested that an increase in circulating acetate and liver hypoxia may mediate the effects of alcohol by increasing tissue and interstitial adenosine levels.
Adenosine↗
Measuring alcohol in vapours above the eye.
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Adult↗
Blood acetaldehyde and the ethanol-induced increase in splanchnic circulation.
Acute oral administration of ethanol significantly increases (50-60%) portal blood flow to the liver. As earlier studies have indicated that this effect is maximal at concentrations of ethanol that saturate the alcohol dehydrogenase (ADH) system and is blocked by the ADH inhibitor 4-methylpyrazol, we investigated the possible role of acetaldehyde, a product in the ADH reaction, as a mediator of this effect. In the first series of experiments it was shown that, contrary to expectations, cyanamide administration prior to alcohol suppressed fully the effect of ethanol on portal blood flow without altering it in the absence of ethanol [ethanol = 69.5 +/- 5.6; ethanol + cyanamide 42.9 +/- 2.4; control = 43.0 +/- 3.0; cyanamide = 55.1 +/- 3.7 ml X min-1 X (kg body wt)-1]. Arterial blood concentrations of acetaldehyde were elevated from 3.6 +/- 0.3 microM in the presence of ethanol to 293 +/- 48 microM in the presence of ethanol + cyanamide. Infusion of acetaldehyde either into the left ventricle, resulting in arterial blood acetaldehyde levels of 227 +/- 77 microM, or into the portal circulation, resulting in arterial blood levels of 198 +/- 40 microM, did not modify portal blood flow or splanchnic hemodynamics, nor the effect of ethanol per se. The combination of cyanamide + ethanol significantly reduced total peripheral resistance (from 28 +/- 3 to 19 +/- 2 dyne X cm X sec-5), while neither ethanol or cyanamide per se, nor acetaldehyde affected total peripheral resistance. Data suggest that acetaldehyde is not involved in the ethanol-mediated increase in portal vein flow. Further studies indicate that the effects of cyanamide in suppressing the ethanol-induced increase in portal blood flow and increasing total peripheral resistance appear to be related to an ethanol-cyanamide interaction which is independent of the acetaldehyde levels in the circulation.
Acetaldehyde↗
Ethanol vapor above skin: determination by a gas sensor instrument and relationship with plasma concentration.
Studies with a new instrument show that blood ethanol concentrations in rats and humans can be estimated by measurement of ethanol vapor above the skin. After intravenous bolus administration of ethanol (1 g/kg) to rats a novel device based on the Figaro sensor was placed above the animal's abdomen. Plasma and skin vapor ethanol concentrations, analyzed by gas chromatography and sensor, respectively, declined in parallel (r = 0.96). In healthy human subjects, plasma and skin vapor concentrations, measured on the palm, also declined in parallel after intravenous ethanol infusion (1 hr, 0.5 g/kg), r = 0.99. In 10 alcoholic liver disease outpatients attending clinic in whom plasma ethanol concentrations ranged from 32-304 mg/dl, the correlation of plasma ethanol determined directly by gas chromatography and indirectly by skin vapor analysis was slope = 0.93, intercept = 1.8, r = 0.94. In controlled studies, skin vapor measurements are comparable with breathalyzer determinations; they may be performed in situations where breathalyzer measurements are inconvenient or where continuous monitoring is desirable.
Adult↗
Ethanol vapours above lacrimal fluid in the rabbit.
Ethanol was administered intravenously to rabbits. The concentration of ethanol, determined by gas chromatographic analysis, in lacrimal fluid was shown to reflect the concentration in plasma. The vapour above lacrimal fluid was analyzed in situ by the use of a small resistivity sensor that measures ethanol vapours. After a dose of approximately 750 mg/kg, the metabolic rates of ethanol determined by gas chromatographic analysis of plasma (226 +/- 13 mg.kg-1.h-1) and by eye ethanol vapour analysis (210 +/- 8 mg.kg-1.h-1) were virtually identical. The data suggest that ethanol eye vapour analysis may be an attractive, noninvasive method for the determination of ethanol in animals.
Animals↗
New instrument using gas sensors for the quantitative analysis of ethanol in biological liquids.
A gas sensor was built into an instrument to measure ethanol in biological liquids by determining head space ethanol concentrations without chromatography. The analysis of plasma, urine, and whole blood containing ethanol over the range 20-640 mg/dl determined by this novel instrument is fast (30 sec), accurate (r = 0.99), and precise (coefficients of variation 0.6-1.8%) when compared with gas chromatography. The addition of alcohol dehydrogenase, beta-nicotinamide adenine dinucleotide, and semicarbazide to samples allows ethanol to be distinguished from other alcohols. The instrument can be built and operated at modest costs thus allowing its use in multiple settings.
Alcohol Dehydrogenase↗
Semiautomated analysis of ethanol and acetate in human plasma by head space gas chromatography.
Plasma samples (0.5 mL) were analyzed for ethanol and acetate by head space gas chromatography using a Porapak QS column (80-100 mesh). Acetate was esterified to methyl acetate simply by the addition of acidified methanol. The analytical ranges were 1.61-103 and 0.05-1.9 mM for ethanol and acetate, respectively. The within-run coefficients of variation did not exceed 4.7% for acetate and 2.7% for ethanol. After the oral administration of ethanol to two healthy human subjects, the concentration versus time profiles of plasma ethanol and acetate were determined. Acetate concentrations (0.4-0.9 mM) remained quite constant while ethanol was being metabolized and appeared not to be affected by the concentration of ethanol in the range 3-18 mM. The advantages of the method are speed and simplicity.
Acetates↗
Lack of changes in diene conjugate levels following ethanol induced glutathione depletion or hepatic necrosis.
Acute administration of 5 g/kg ethanol resulted in a 35% reduction of glutathione levels but not in increases in lipoperoxidation as measured by diene conjugate levels in mitochondria or in microsomes. Administration of diethylmaleate which markedly decreased glutathione levels by 85% did not render the livers susceptible to lipoperoxidation after ethanol administration. Chronic alcohol administration did not result in detectable changes in diene conjugates with respect to isocaloric sucrose treatment. Liver necrosis when induced by anemia in rats chronically treated with ethanol was not accompanied by increases in diene conjugate levels.
Animals↗
Condensation of isoniazid and acetaldehyde.
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Acetaldehyde↗
Effect of alcohol on propylthiouracil disposition.
We examined the effect of ethanol on propylthiouracil (PTU) disposition in normal subjects and a rabbit. The drug is metabolized by conjugation. In six normal subjects 19.2 gm oral ethanol, taken either with or two hr after 300 mg PTU, did not change maximum concentration, time to maximum concentration, or total or free AUC of PTU. Pretreatment with ethanol and supplementation to keep blood ethanol concentration above 800 mg/l for 8 hr also did not alter PTU disposition. In the rabbit, the infusion of ethanol (8.81 mg/min) 4 hr after the beginning of an intravenous infusion of PTU 0.05 mg/min did not alter the plasma concentration profile. These results indicate that short-term ethanol dosing does not affect PTU disposition and therefore dosage adjustment is not necessary in patients who drink alcohol.
Administration, Oral↗
In vitro quantitation of benzodiazepine lipophilicity: relation to in vivo distribution.
In vitro lipophilicity of a series of benzodiazepines was evaluated by octanol: buffer partition ratio at physiological pH, and by retention time on a reverse-phase high-pressure liquid chromatographic (HPLC) system with a neutral-pH mobile phase. Both approaches ranked diazepam as highly lipophilic, but overall the two indices were poorly correlated (r = 0.23). For seven of the benzodiazepines, the in vivo volume of distribution (Vd) was determined in pharmacokinetic studies. After correlation for individual values of protein binding, Vd for unbound drug was significantly correlated with octanol: buffer partition ratio (r = 0.74), and to a greater extent with HPLC retention (r = 0.81). Thus, lipid solubility at least partly determines the extent of benzodiazepine distribution in vivo, which in turn is a major determinant of the duration of clinical action after single doses.
Adult↗
Diazepam pharmacokinetics after intravenous administration in alcohol withdrawal.
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Adult↗
Artifactual production and recovery of acetaldehyde from ethanol in urine.
Ethanol (1575 mg/L) incubated with fresh urine from healthy, ethanol-free subjects yields acetaldehyde. The concentration of acetaldehyde depends upon temperature, time of incubation, and pH. In samples made hypertonic with sodium chloride (200 mg/mL) and in samples filtered through 0.45-micron membranes, acetaldehyde production was not decreased. L-Ascorbic acid (0.1 mg/mL) added to normal pooled urine caused a threefold increase in acetaldehyde production but thiourea (7.6 mg/mL) stopped it. This suggests that the oxidation of ethanol to acetaldehyde is catalyzed by the semidehydroascorbate peroxy radical of ascorbic acid. Recovery of acetaldehyde added to urine was less than 100% over the pH range 1.5 to 10. Relative to blood, artifactual production of acetaldehyde from ethanol in urine is more easily controlled and is up to an order of magnitude less but corrections for the variables above are still required.
Acetaldehyde↗