Blood Ethanol Levels Research Articles

Food from Equids-Commercial Fermented Mare's Milk (Koumiss) Products: Protective Effects against Alcohol Intoxication.

Fermented mare's milk (koumiss), a traditional Central Asian dairy product derived from fermented mare's milk, is renowned for its unique sour taste and texture. It has long been consumed by nomadic tribes for its nutritional and medicinal benefits. This study aimed to comprehensively analyze the protective effects of koumiss against alcohol-induced harm across behavioral, hematological, gastrointestinal, hepatic, and reproductive dimensions using a mouse model. Optimal intoxicating doses of alcohol and koumiss doses were determined, and their effects were explored through sleep tests and blood indicator measurements. Pretreatment with koumiss delayed inebriation, accelerated sobering, and reduced mortality in mice, mitigating alcohol's impact on blood ethanol levels and various physiological parameters. Histopathological and molecular analyses further confirmed koumiss's protective role against alcohol-induced damage in the liver, stomach, small intestine, and reproductive system. Transcriptomic studies on reproductive damage indicated that koumiss exerts its benefits by influencing mitochondrial and ribosomal functions and also shows promise in mitigating alcohol's effects on the reproductive system. In summary, koumiss emerges as a potential natural agent for protection against alcohol-induced harm, opening avenues for future research in this field.

HISTOSTRUCTURAL ALTERATIONS IN THE CEREBRAL ARCHITECTURE ASSOCIATED WITH THE PROGRESSION OF ALCOHOL INTOXICATION: AN EXPERIMENTAL ANALYSIS

The aim of this study is to evaluate the histological changes in the cerebellum of rat brains following chronic alcohol intoxication. Materials and Methods. We employed a classical approach for modeling chronic alcohol intoxication by administering 40% ethanol to rats (n=55) in a dosage of 2 ml per 100 g of body weight daily for three months. The cerebellar structure was then analyzed. Results. This study investigates the impact of chronic alcohol intoxication on the histological structures of the cerebellar cortex. The cerebellum, like the nervous system overall, possesses a significant cellular and functional reserve. However, teratogenic factors, including ethanol, notably influence the activity of cerebellar neurons, increasing it. Ethanol exposure during early pregnancy can lead to prenatal growth retardation, stillbirth, cleft palate, hydrocephaly, and reductions in fetal body size. There is evidence suggesting a correlation between blood ethanol levels and a reduction in the number of Purkinje cells. Chronic alcohol consumption results in cerebellar ataxia, alterations in upper limb movements, decreased reaction speeds, reduced attention concentration, impaired coordination accuracy, and disturbances in postural stability and balance. Conclusion. The cerebellum, especially during development, is particularly vulnerable to the toxic effects of alcohol. Recent research suggests that changes in the neurotransmission of gamma-aminobutyric acid (GABA)-dependent receptors may contribute to cerebellar dysfunction induced by ethanol. Ethanol exposure increases the release of GABA not only in Purkinje cells but also in the interneurons of the molecular layer and granule cells.

Proposal of a New Predictive Score for the Requirement of Intensive Care Unit Admission Among Ethanol-Intoxicated Patients

ABSTRACT The correct selection of ethanol-intoxicated patients that require ICU admission is crucial for reducing morbidity and mortality. This study included 165 patients intoxicated with ethanol, confirmed by blood analysis. The patients were divided into ICU group = 46 and inward group = 119. We created a new predictive score based on seven parameters of APACHE II score and seven laboratory parameters that were significant in ICU-admitted patients by giving each parameter one point. The new predictive score achieved a sensitivity of 87, a specificity of 93.3, and an area under the curve of 0.967 with a cutoff >6. On the other hand, blood ethanol level (BEL) exhibited a weak correlation with both APACHE II and new predictive scores and a weak correlation with the parameters of the new predictive score. The new predictive score included 14 parameters. This score can be used in predicting whether patients need ICU admission during assessment for ethanol intoxication in emergency rooms, independent of BEL analysis. It could potentially reduce morbidity and mortality.

Melatonin reduces brain injury following inflammation-amplified hypoxia-ischemia in a translational newborn piglet study of neonatal encephalopathy.

There is a need to develop therapies for neonatal encephalopathy (NE) in low- and middle-income countries (LMICs) where the burden of disease is greatest and therapeutic hypothermia (HT) is not effective. We aimed to assess the efficacy of melatonin following inflammation-amplified hypoxia-ischaemia (IA-HI) in the newborn piglet. The IA-HI model accounts for the contribution of infection/inflammation in this setting and HT is not cytoprotective. We hypothesised that intravenous melatonin (5% ethanol, at 20 mg/kg over 2 h at 1 h after HI + 10 mg/kg/12 h between 24 and 60 h) is safe and associated with: (i) reduction in magnetic resonance spectroscopy lactate/N-acetylaspartate (MRS Lac/sNAA); (ii) preservation of phosphorus MRS phosphocreatine/phosphate exchange pool (PCr/Epp); (iii) improved aEEG/EEG recovery and (iv) cytoprotection on immunohistochemistry. Male and female piglets underwent IA-HI by carotid artery occlusion and reduction in FiO2 to 6% at 4 h into Escherichia coli lipopolysaccharide sensitisation (2 μg/kg bolus + 1 μg/kg/h over 12 h). At 1 h after IA-HI, piglets were randomised to HI-saline (n = 12) or melatonin (n = 11). There were no differences in insult severity between groups. Target melatonin levels (15-30 mg/L) were achieved within 3 h and blood ethanol levels were <0.25 g/L. At 60 h, compared to HI-saline, melatonin was associated with a reduction of 0.197 log10 units (95% CrI [-0.366, -0.028], Pr(sup) 98.8%) in basal-ganglia and thalamic Lac/NAA, and 0.257 (95% CrI [-0.676, 0.164], Pr(sup) 89.3%) in white matter Lac/NAA. PCr/Epp was higher in melatonin versus HI-saline (Pr(sup) 97.6%). Melatonin was associated with earlier aEEG/EEG recovery from 19 to 24 h (Pr(sup) 95.4%). Compared to HI-saline, melatonin was associated with increased NeuN+ cell density (Pr(sup) 99.3%) across five of eight regions and reduction in TUNEL-positive cell death (Pr(sup) 89.7%). This study supports the translation of melatonin to early-phase clinical trials. Melatonin is protective following IA-HI where HT is not effective. These data guide the design of future dose-escalation studies in the next phase of the translational pipeline.

MASLD is related to impaired alcohol dehydrogenase (ADH) activity and elevated blood ethanol levels: Role of TNFα and JNK

Elevated fasting ethanol levels in peripheral blood frequently found in metabolic dysfunction-associated steatohepatitis (MASLD) patients even in the absence of alcohol consumption are discussed to contribute to disease development. To test the hypothesis that besides an enhanced gastrointestinal synthesis a diminished alcohol elimination through alcohol dehydrogenase (ADH) may also be critical herein, we determined fasting ethanol levels and ADH activity in livers and blood of MASLD patients and in wild-type ± anti-TNFα antibody (infliximab) treated and TNFα-/- mice fed a MASLD-inducing diet. Blood ethanol levels were significantly higher in patients and wild-type mice with MASLD while relative ADH activity in blood and liver tissue was significantly lower compared to controls. Both alterations were significantly attenuated in MASLD diet-fed TNFα-/- mice and wild-type mice treated with infliximab. Moreover, alcohol elimination was significantly impaired in mice with MASLD. In in vitro models, TNFα but not IL-1β or IL-6 significantly decreased ADH activity. Our data suggest that elevated ethanol levels in MASLD patients are related to TNFα-dependent impairments of ADH activity.

Analysis of Punch Injuries: Clinical Characteristics, Management and Outcomes.

The aim of this study is to describe injury patterns, characteristics, treatment modalities and functional outcomes after punching related injuries. Retrospective data of cases admitted to emergency department following punch injury between January 1, 2012, and December 31, 2022. was collected. Patient's demographic data, the dominant and injured upper extremity side, punched object, a time of patient admission were recorded. Smoking habit and blood ethanol level were documented. Trauma mechanism, diagnosis (1: dermabrasions: skin, 2: lacerations: neurovascular structures or tendons and 3: osseous pathologies), treatment modalities were analyzed. Outcomes were assessed using the DASH questionnaire (Disabilities of the Arm, Shoulder, and Hand) at the last follow-up. A total of 1052 patients (male=968 (92%), female=84 (8%)) with mean age 24.6 ± 7.2 included this study. Six hundred and twenty-one (59%) patients punched a solid object and 675 (64%) had osseous pathology. The most commonly fractured bone, injured tendon, injured nerve, and injured artery were 5th metacarpal, extensor digitorum communis (EDC), ulnar nerve, and ulnar artery, respectively. The majority of the patients, (73%) were smokers while 15% of the patients had high level of blood ethanol concentration on admission (82±12.3 mg/100 ml). A comparison between smokers and non-smokers did not reveal any significant differences (p=0.425) in terms of diagnosis whereas 74% of alcoholic patients admitted with lacerations which was statistically significant (p=0.023). Injuries of 321 (30.5%) patients required surgery in the operating room, while 711(67.5 %) patients received interventions in the emergency room setting. The average DASH score differed between subgroups, with significantly higher scores in patients with laceration type injuries (7.2 SD), indicating more disability (p=0.001) DISCUSSION. The study reveales a high prevalence of hand injuries among individuals aged 18 to 40, with the dominant hand being most affected, primarily due to physical violence and self-harming behaviors. Primary contributing factors to this pattern are the escalated incidents of physical violence and self-harming behaviors arising from an inability to manage anger impulses. Punching solid objects, especially during late afternoon and evening periods often associated with alcohol use, was a common cause, resulting in metacarpal fractures being the most reported injury. Multiple tendon and nerve injuries were frequent, highlighting the severity and complexity of these traumas, often necessitating surgical intervention. These findings highlight the several key aspects, including demographic characteristics of the patient population, common causes and types of injuries observed, and the association between alcohol use as well as the specific injury profiles. Satisfactory results can be achieved with both conservative and surgical treatment for punch injuries. punching, fisting, boxing injuries, laceration, blood ethanol level.

Defecation alleviates hangover by terminating intestinal drinking.

The concept of "intestinal drinking" in this study refers to the continued absorption of alcohol in the gastrointestinal tract until adequate defecation occurs. A longitudinal observation of hangover symptoms and alcohol metabolites in healthy humans following binge drinking was conducted. The hangover symptoms resulting from binge alcohol consumption were relieved by defecation. Following the defecation process, not only the blood ethanol levels, but also the concentrations of blood acetaldehyde, methanol, and iso-propanol, exhibited significant reductions. This pilot study provides a different perspective for addressing hangovers and potentially mitigating the risks of alcoholic liver diseases.

Juvenile variable stress modulates, in female but not in male Wistar rats, ethanol intake in adulthood

Early stress can increase vulnerability to psychopathological disorders, including substance use disorders. The effects of stress in the juvenile period of the rat, that extends between weaning and the onset of adolescence (equivalent to late human childhood), have received little attention. This study assessed short and long-term behavioral effects of juvenile stress, with a focus on effects on ethanol intake. Male and female Wistar rats were exposed to variable stress (restraint, elevated platform, forced swimming, and social instability) or to restraint stress only, between postnatal days 26 to 29 (PDs 26–29). During adolescence, patterns of anxiety (PD 31) and depression (PD 33), ethanol intake (PDs 36–45) and behavioral sensitivity to the effects of acute stress (PD 47) were evaluated. In adulthood, alcohol ingestion was assessed through two-bottle ethanol intake tests (PDs 75–85). An additional experiment measured blood ethanol levels after a limited access intake session in adolescence. Exposure to juvenile variable stress exerted very mild effects in adolescence, but reduced ethanol ingestion in adulthood, in females only. Ethanol intake during the limited access session was significantly correlated to blood alcohol levels. The results indicate that a schedule of juvenile variable stress that did not significantly alter anxiety-related behaviors induced, nonetheless, sexually dimorphic effects on ethanol intake in adulthood. Early stress exposure that reduced alcohol intake in Wistar rats has been associated with changes on brain opioid and dopamine receptors. These results highlight the impact of early stress exposure on adult female ethanol consumption and its possible underlying neurobiological changes, involving opioid and dopamine receptors.

Pengaruh Kadar Etanol Darah Terhadap Kadar Gamma Glutamyl Transferase (GGT) pada Pekerja Pembuatan Etanol di Desa Ngombakan Polokarto

Ethanol is the result of sugarcane fermentation which is converted into molasses (cane drops). Then the distillation process is carried out by heating for a certain time so that a certain level of ethanol is obtained. The process of making ethanol is an activity that has a high risk for its workers. The heating process produces vapors that are harmful to the body, causing health problems for workers. Liver disease is the most common complication caused by exposure to ethanol. Alcoholic fatty liver is a reversible disease that can progress to alcoholic hepatitis which can cause liver cirrhosis and liver failure. This study was conducted to determine blood ethanol levels, Gamma GT levels and the effect of blood ethanol levels on Gamma GT in ethanol production workers. The research was conducted by quota sampling as many as 24 people in 8 traditional ethanol-making industrial houses in Ngombakan, Polokarto. Ethanol examination was carried out using the Gass Chromatography and Mass Spectrometry method and Gamma GT was carried out using the colorimetric enzymatic method. The results obtained are the average ethanol content of the workers is 0.45 mg/dL and Gamma GT is 29 U/L. The results of linear regression analysis showed Sig. 0.257 (0.05) meaning that there was no effect of ethanol content on Gamma GT levels. Based on the coefficient of determination (R2) of 0.058, it means that the effect of ethanol on Gamma GT is 5.8%.

Effects of Chronic Alcohol Consumption and Iron Deficiency on Maternal Folate Status and Reproductive Outcome in Mice

The influence of chronic alcohol consumption with or without iron deficiency on reproductive performance and folate status was studied. Female CBA/J mice were fed isocaloric liquid diets prior to and during pregnancy. A 2 × 2 factorial design was employed with ethanol-derived calories (EDC) and iron (Fe) as dietary variables. Groups received 0% EDC and 30 ppm Fe (CA); 0% EDC and 2 ppm Fe (CD); 20% EDC and 30 ppm Fe (EA); and 20% EDC and 2 ppm Fe (ED). Animals were killed on day 18 of gestation. Mean body weights were reduced in CD, EA and ED groups, while daily caloric intakes reduced only in CD and ED groups. Maternal values for hemoglobin, transferrin saturation and red cell folates decreased with iron deficiency and/or 20% EDC; hematocrit, serum iron and serum folates decreased only with iron deficiency. Blood ethanol levels were similar in EA and ED groups. Maternal liver total lipids and alcohol dehydrogenase activity increased only with 20% EDC, while dihydrofolate reductase activity decreased with iron deficiency and/or 20% EDC. Iron deficiency and/or 20% EDC adversely affected gestational performances in mice as indicated by increased resorptions and decreased percentages of live fetuses/litters and live fetal weights. Data indicate that iron deficiency and/or chronic ethanol consumption induce adverse effects on maternal reproductive performance of CBA/J mice possibly via alteration of folate metabolism.

Folate administration ameliorates neurobehavioral effects of prenatal ethanol exposure

ABSTRACT Background: Prenatal ethanol exposure (PEE) induces heightened ethanol intake at adolescence in preclinical studies. Ethanol intake alters the absorption of folate, a methyl-group donor critical for numerous cellular functions. The prenatal administration of folate is, therefore, a promising approach to reduce the effects of PEE. Objectives: Experiment 1 determined if prenatal folate modulated the effects of PEE on ethanol intake, anxiety-like response, and exploratory behaviors (Experiment 1) in Wistar rats. Experiment 2 assessed, in rats not given PEE, if postnatal folate reversed effects of ethanol exposure at postnatal days 28–42. Experiment 3 assessed if folate altered blood ethanol levels (BELs). Methods: Experiment 1 involved 242 (125 male) adolescent Wistar rats derived from dams given folate (20 mg/kg, gestational days – GD- 13-20) + ethanol (2.0 g/kg, GD 17–20), ethanol, or vehicle only at pregnancy. Experiment 2 involved 29 male adolescents administered vehicle or ethanol doses co-administered or not with folate. In Experiment 3 twelve adult females were tested for BELs after folate administration. These tests were applied: intake tests, light dark box (LDB), elevated plus maze, open field and concentric square field. Results: PEE heightened ethanol intake (η2 ps = 0.06–07) and induced hyperactivity and a reduced latency to exit the white area of the LDB (η2 ps = 0.12–17). These effects were partially inhibited by folate (p > .05). Rats exposed to ethanol exposure at adolescence exhibited reduced motor activity (η2 p = .17), regardless of folate treatment. Folate did not affect BELs. Conclusion: Folate administration should be considered as a preventive or acute treatment to attenuate the neurobehavioral effects of PEE.

Ethyl sulfate in blood shows the potential to distinguish alcoholic death and postmortem alcohol instillation

Alcohol is often found in the blood of the deceased. To cover up the true cause of victim’s death, postmortem instillation of alcohol occurs in some criminal cases. Explaining the finding of alcohol is extremely vital in forensic practice. This study aims to evaluate whether ethyl glucuronide (EtG) and ethyl sulfate (EtS) in blood and vitreous humor (VH) can be used to distinguish alcoholic death and postmortem alcohol instillation. Saline or 12.6 g/kg ethanol (antemortem alcohol poisoning group) was introduced into rabbits’ stomachs 2 h before sacrificed. Same amount of ethanol was introduced into rabbits’ stomachs at 0 h, 0.5 h, 1 h and 2 h after death in four subgroups of postmortem alcohol instillation group, respectively. Cardiac blood and VH were collected at 10 min, 4 h, 10 h and 24 h after death in blank and antemortem alcohol poisoning group, and after instillation of alcohol in postmortem alcohol instillation group. Blood was also collected at 34 h. Ethanol and EtG levels in blood and VH and EtS in VH in antemortem alcohol poisoning group were overlapped with those in postmortem alcohol instillation group. The contents of EtG and EtS in blood in antemortem alcohol poisoning group (mean ≥ 7.833 μg/mL for EtG and ≥ 19.990 μg/mL for EtS) were much higher than those in postmortem alcohol instillation group (mean ≤ 0.118 μg/mL for EtG and ≤ 0.091 μg/mL for EtS), but apparent decomposition was observed in EtG, which might lead to misinterpretation. Blood EtS showed better stability and could be used to distinguish alcoholic death and postmortem alcohol instillation.

PSUN279 Refractory Hypoglycemia in the Setting of Incidental Urothelial Carcinoma

Abstract Introduction Hypoglycemia is uncommon in individuals who do not have drug-treated diabetes mellitus. In such patients, differentials include cortisol deficiency, insulinomas or autoantibodies against insulin/ insulin receptor. Malignancy related causes include non-islet cell tumors and extensive liver infiltration. This case highlights the workup of hypoglycemia in a patient with an incidental diagnosis of urothelial cancer. Clinical Case We present a 62 year old male who was assessed by the EMS at home for difficulty in arousal and facial drooling. Initial assessment found him to have a random glucose of 26mg/dL. His glucose was corrected with dextrose and the EMS left. Nine hours later the EMS was called again strange behavior, where he was found again to be hypoglycemic (19mg/dL). Glucagon and dextrose was administered and he was transported to the ED. His finger stick glucose on arrival was 26mg/dL. Endocrine history is primary hypothyroidism only. Other significant past medical history was a retroperitoneal mass seen on routine surveillance imaging one month ago, after being treated for renal cell carcinoma with right partial nephrectomy 10 years ago. On physical exam, vitals were stable, he was alert and oriented. Other physical examination findings were normal. His BMI was 35.23 kg/m2. Relevant initial labs were venous blood glucose 43 mg/dL, TSH 11.4 uU/mL and T4 was 1.1 ng/dL. Blood ethanol level was undetectable. Despite receiving multiple ampules of 50% dextrose and continuous 10-20% dextrose IV infusion he continued to be hypoglycemic and therefore was admitted to the ICU. The initial management course was as follows: He was started on octreotide infusion and given scheduled diazoxide for persistent hypoglycemia with no improvement. For suspected non-islet cell tumor, he was started on glucagon infusion, however there was no significant correction. Calorie intake was monitored and increased by nutrition and was subsequently given enteral/ parenteral nutrition. He was also started on hydrocortisone 50mg every 8 hours. Endocrine investigations were as follows: Insulin, C-peptide, urine sulfonylureas and ß-hydroxybutyrate were undetectable, proinsulin 2.9 pmol/L (ref &amp;lt;= 8.0 pmol/L), Insulin antibody negative, IGF-1 44 ng/mL (ref 49-214 ng/mL), IGF-2 129 ng/dL (IGF-II/IGF-I &amp;lt; 10). Random cortisol was 26 µg/dL. Investigations for the retroperitoneal mass were as follows: a biopsy showed high grade invasive urothelial carcinoma. MRI abdomen showed extensive and diffuse infiltrative metastatic liver disease without evidence of pancreatic endocrine tumor. The final diagnosis was determined to be due to extensive tumor infiltration in the liver. His condition deteriorated during ICU stay and comfort measures were initiated; subsequently he deceased. Conclusion The causes of hypoglycemia in patients with known tumors include extensive tumor infiltration and nonislet cell tumors, two uncommon causes of hypoglycemia. Differentiating between nonislet tumor secretion and direct tumor infiltration is based on IGF-2 level and the IGF-2/IGF-1 ratio. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.

Hepatic CYP2B10 is highly induced by binge ethanol and contributes to acute-on-chronic alcohol-induced liver injury.

The chronic-plus-binge model of ethanol consumption, where chronically (8-week) ethanol-fed mice are gavaged a single dose of ethanol (E8G1), is known to induce steatohepatitis in mice. However, how chronically ethanol-fed mice respond to multiple binges of ethanol remains unknown. We extended the E8G1 model to three gavages of ethanol (E8G3) spaced 24 h apart, sacrificed each group 9h after the final gavage, analyzed liver injury, and examined gene expression changes using microarray analyses in each group to identify mechanisms contributing to liver responses to binge ethanol. Surprisingly, E8G3 treatment induced lower levels of liver injury, steatosis, inflammation, and fibrosis as compared to mice after E8G1 treatment. Microarray analyses identified several pathways that may contribute to the reduced liver injury after E8G3 treatment compared to E8G1 treatment. The gene encoding cytochrome P450 2B10 (Cyp2b10) was one of the top upregulated genes in the E8G1 group and was further upregulated in the E8G3 group, but only moderately induced after chronic ethanol consumption, as confirmed by RT-qPCR and western blot analyses. Genetic disruption of Cyp2b10 worsened liver injury in E8G1 and E8G3 mice with higher blood ethanol levels compared to wild-type control mice, while in vitro experiments revealed that CYP2b10 did not directly promote ethanol metabolism. Metabolomic analyses revealed significant differences in hepatic metabolites from E8G1-treated Cyp2b10 knockout and WT mice, and these metabolic alterations may contribute to the reduced liver injury in Cyp2b10 knockout mice. Hepatic Cyp2b10 expression is highly induced after ethanol binge, and such upregulation reduces acute-on-chronic ethanol-induced liver injury via the indirect modification of ethanol metabolism.

Alcohol and children: clinical and forensic study

BACKGROUND: This study aimed to evaluate the differences in the clinical pictures in the group of alcohol intoxication (without the loss of conscious) and alcohol poisoning (with the loss of conscious).&#x0D; AIMS: This study aimed to investigate the clinical differences in the groups of alcohol intoxication (without loss of consciousness) and alcohol poisoning (with loss of consciousness) and determine the level of blood ethanol concentrations in children and adolescents from alcohol intake that causes a loss of consciousness, which means ethanol poisoning occurrence, and finally, offer practical recommendations for forensic doctors in cases of alcohol poisoning in children.&#x0D; MATERIALS AND METHODS: The total amount of data was a combination of two studied populations: population No. 1 from the archive of the Bureau and population No. 2 from the Childrens Clinical Hospital No. 13 named after N.F. Filatov. The study is a retrospective population-based and prospective (observational) cross-sectional study. Data were grouped as (1) persons whose alcohol intake did not cause significant health disorders (alcohol intoxication) and (2) persons whose alcohol intake caused the onset of coma, respiratory arrest, or death (alcohol poisoning). Urine screening for psychoactive and narcotic substances was conducted using liquid chromatography-tandem mass spectrometry.&#x0D; RESULTS: The data set included 67 minors aged 1117 years. Blood and urine ethanol levels of males and blood of females were significantly higher than in patients with alcohol intoxication. The objective status of patients was the same. No differences were found in alcohol pharmacokinetics (resorption and elimination), as well as the instrumental parameter readings. The present study revealed that alcohol intoxication and poisoning were not associated with dangerous changes in such parameters as systolic blood pressure, diastolic blood pressure, heart rate, and respiratory rate.&#x0D; CONCLUSION: The results showed that ethanol poisoning in children aged 1117 years old developed at an ethanol concentration of 2.61 g/L in the blood and 3.01 g/L in the urine. Additionally, no significant differences were found in the instrumental parameters.

Review of Ethanol Intoxication Sensing Technologies and Techniques.

The field of alcohol intoxication sensing is over 100 years old, spanning the fields of medicine, chemistry, and computer science, aiming to produce the most effective and accurate methods of quantifying intoxication levels. This review presents the development and the current state of alcohol intoxication quantifying devices and techniques, separated into six major categories: estimates, breath alcohol devices, bodily fluid testing, transdermal sensors, mathematical algorithms, and optical techniques. Each of these categories was researched by analyzing their respective performances and drawbacks. We found that the major developments in monitoring ethanol intoxication levels aim at noninvasive transdermal/optical methods for personal monitoring. Many of the “categories” of ethanol intoxication systems overlap with each other with to a varying extent, hence the division of categories is based only on the principal operation of the techniques described in this review. In summary, the gold-standard method for measuring blood ethanol levels is through gas chromatography. Early estimation methods based on mathematical equations are largely popular in forensic fields. Breath alcohol devices are the most common type of alcohol sensors on the market and are generally implemented in law enforcement. Transdermal sensors vary largely in their sensing methodologies, but they mostly follow the principle of electrical sensing or enzymatic reaction rate. Optical devices and methodologies perform well, with some cases outperforming breath alcohol devices in terms of the precision of measurement. Other estimation algorithms consider multimodal approaches and should not be considered alcohol sensing devices, but rather as prospective measurement of the intoxication influence. This review found 38 unique technologies and techniques for measuring alcohol intoxication, which is testament to the acute interest in the innovation of noninvasive technologies for assessing intoxication.

Hippocampal Physiological and Behavioral Deficits Related to Alcohol‐induced Disruption of Local Blood Perfusion

Despite preventative education, moderate‐heavy episodic alcohol (ethanol; EtOH) intake, such as in “binge” drinking, remains a major public health problem. Binge drinking, can lead to blood ethanol levels above legal intoxication and cause alcohol‐induced blackouts (AIB), a form of amnesia linked to dysfunction of the hippocampal CA1 region. The neurobiological bases of AIB, however, remain largely unknown. It is noteworthy that proper function of neurons in the brain, including the CA1 region, critically depends on aerobic metabolism and optimal blood flow (BF). Using rodent models, we previously showed that EtOH at intoxicating concentrations constricted cerebral arteries independently of circulatory, metabolic, and endothelial factors, but due to drug inhibition of large conductance Ca2+‐ and voltage‐gated K+ (BK) channels present in vascular smooth muscle. Using behavioral modeling of contextual fear conditioning with miniscope technology, the present study tests the hypothesis that EtOH‐induced anterograde memory dysfunction is coincidental to EtOH‐induced reduction in local blood flow and reduced neuronal activity in the CA1 region. Thus, we used Ca2+‐release imaging to map single neuron activity in combination with dynamic local BF recordings in awake and freely moving mice to simultaneously determine vascular, neurophysiological and behavioral effects of EtOH in a mouse model of AIB. Ca2+ imaging was conducted using GCaMP6, which provided a blue fluorescent light when neurons released Ca2+, indicating action potentials, while rhodamine dextran dye provided a red label for the vasculature within the CA1. AIB was modeled via contextual fear conditioning, in which mice were exposed to electric shocks after receiving intraperitoneal injections (IP) of saline or EtOH. Twenty‐four hours later, animals were placed into the same boxes, and their freezing behavior was recorded. Data revealed that IP injection of 2 mg/kg EtOH evoked a robust (&gt;50%) decrease in Ca2+ fluorescence which was coincidental to an 18% decrease in cerebral artery diameter. Reductions in neuronal activity and cerebral artery diameter were, indeed, accompanied by a 42.3% reduction in freezing behavior (P&gt;0.05). Thus, this study identifies both vascular and neurophysiological components of EtOH action on the hippocampus CA1 region in a behavioral model of AIB. More generally, our study is the first to investigate the simultaneous effects of EtOH on behavior, including anterograde memory, neuronal activity, and local BF dynamics in the brain.

Ethanol consumption activates a subset of arcuate nucleus pro-opiomelanocortin (POMC)-producing neurons: a c-fos immunohistochemistry study.

Ethanol activates various opioid peptide‐containing circuits within the brain that may underlie its motivational and rewarding effects. One component of this circuitry consists of neurons located in the arcuate nucleus (ArcN) of the hypothalamus which express pro‐opiomelanocortin (POMC), an opioid precursor peptide that is cleaved to form bioactive fragments including β‐endorphin and α‐melanocyte stimulating hormone. In this study, we sought to determine if ethanol intake activates ArcN POMC neurons as measured by expression of the immediate early gene c‐fos. Male and female POMC‐EGFP mice underwent drinking‐in‐the‐dark (DID) procedures for 3 consecutive days (2 h/day) and were allowed to consume either ethanol (20% v/v), saccharin (0.2% w/v), or water. On the fourth day of DID procedures, animals were allowed to consume their respective solutions for 20 min, and 1 h following the session brains were harvested and processed for c‐fos immunohistochemistry and co‐localization with EGFP. Our results indicate that ethanol intake activates a subset (~15–20%) of ArcN POMC neurons, whereas saccharin or water intake activates significantly fewer (~5–12%) of these neurons. The percent of activated POMC neurons did not correlate with blood ethanol levels at the time of tissue collection, and activation appeared to be distributed throughout the rostrocaudal axis of the ArcN. No sex differences were observed in the degree of neuronal activation across drinking solutions. These findings indicate a preferential activation of ArcN POMC neurons by ethanol consumption, strengthening the notion that ethanol activates endogenous opioid systems in the brain which may underlie its motivational properties.

From binge eating to binge drinking: A new and robust paradigm for assessing binge ethanol self-administration in male rats.

Animal models of alcohol (ethanol) self‐administration are crucial to dissect the neurobiological mechanisms underlying alcohol dependence, yet only a few of these induce pharmacologically relevant levels of alcohol consumption and rarely the alcohol self‐administration co‐occurs with other addictive behaviours. The present study aims to validate a novel model of voluntary ethanol consumption in male Wistar rats, in which ethanol access follows a binge eating experience. Over 10 sessions, Wistar rats were exposed to binge or control eating (i.e., the ingestion of 11.66 and 0.97 kcal/3 min, respectively, derived from a highly palatable food), immediately followed by two‐bottle choice intake tests (2%, 6%, 10% or 14% w/w ethanol vs. water). Rats exposed to binge eating drank significantly more 6% or 10% (w/w) ethanol than control peers, reaching up to 6.3 gEtOH/kg. Rats stimulated with 2%, 6%, 10% or 14% ethanol after binge eating, but not those given those ethanol concentrations after control eating, exhibited significant within‐group increases in ethanol drinking. This ethanol consumption was not altered by quinine adulteration (up to 0.1 g/L), and it was blocked by naltrexone (10 mg/kg), administered immediately before binge eating. Blood ethanol levels significantly correlated with ethanol consumption; and the more ethanol consumed, the greater the distance travelled in an open field test conducted after the two‐bottle choice test. Altogether, this self‐administration model seems a valid and robust alternative with remarkable potential for research on different stages of the alcohol addiction and, particularly, to assess interactions between alcohol consumption and others addictive‐like behaviours.

Pairing food and drink: A physiological model of blood ethanol levels for a variety of drinking behaviors

We present a blood ethanol concentration compartment model which utilizes an animal’s ethanol intake, food intake, and weight to predict the animal’s blood ethanol concentration at any given time. By incorporating the food digestion process into the model we can predict blood ethanol concentration levels over time for a variety of drinking and eating scenarios. The model is calibrated and validated using data from cohorts of male monkeys, and is able to capture blood ethanol concentration kinetics of the monkeys from a variety of drinking behavior classifications.