乙酰半胱氨酸对小鼠酒精中毒的影响

目的 :观察5 %N—乙酰—L—半胱氨酸 (NAC)口服液对小鼠醉酒后血清乙醇浓度和肝、胃组织乙醇脱氢酶活性的影响。方法 :用生理盐水或5 %NAC口服液灌服小鼠30min后 ,再灌服白酒 ,记录小鼠翻正反射消失 (醉酒 )至恢复 (醒酒 )所需时间及24h内小鼠的死亡只数 ;另对小鼠以相同灌服方法连续6d灌服后眼眶取血并处死小鼠 ,立即取出其肝脏和胃 ,分别用生化比色法测定血清乙醇浓度和肝、胃组织乙醇脱氢酶活性。结果 :在醉酒实验中 ,与对照组比较 ,服用5 %NAC口服液组小鼠从饮酒到醉酒的时间明显延长 (P<0 01) ,醒酒时间明显缩短 ,且小鼠的死亡率明显降低 (P<0 05) ;服用5 %NAC口服液组小鼠血清乙醇浓度明显低于单纯服用白酒的小鼠 (P<0 01)。结论 :5 %NAC口服液具有解酒作用。     

酸奶番茄汁对急性酒精中毒小鼠解酒作用的实验研究

目的：研究酸奶番茄汁的解酒毒作用及其机制。方法：测定服用酸奶番茄汁前后小鼠翻正反射消失和恢复时间、血清乙醇浓度及小鼠肝、胃细胞匀浆中乙醇脱氢酶的活力变化。结果：酸奶番茄汁可缩短翻正反射恢复时间．降低醉酒小鼠血清乙醇含量,提高肝、胃组织乙醇脱氢酶的活性,且比单用酸奶和番茄汁效果更好。结论：酸奶番茄汁对预防和治疗醉酒有较好的作用,其饥制与增强肝脏对乙醇的生物转化功能及降解乙醇有关。     

醒酒浓缩液的药效学研究

目的观测醒酒浓缩液对醉酒小鼠防醉和解酒作用。方法采用醉酒模型并测试小鼠翻正反射消失时间及恢复时间（min），气相色谱检测血中乙醇含量。结果(1)30mL/kg、40mL/kg醒酒浓缩液对醉酒小鼠具有明显防醉和解酒作用（P<0.05～0.01）；（2）醉酒前给小鼠ig醒酒浓缩液，中、高剂量组能明显降低酒后40～120min内血液中乙醇含量（P<0.05～0.01）。结论本品具有较好预防醉酒和解酒作用，其作用机理可能与其降低血中乙醇含量有关。     

醒酒浓缩液的药效学研究

目的观测醒酒浓缩液对醉酒小鼠防醉和解酒作用.方法采用醉酒模型并测试小鼠翻正反射消失时间及恢复时间(min),气相色谱检测血中乙醇含量.结果 (1)30mL/kg、40mL/kg醒酒浓缩液对醉酒小鼠具有明显防醉和解酒作用(P<0.05～0.01);(2)醉酒前给小鼠ig醒酒浓缩液,中、高剂量组能明显降低酒后40～120min内血液中乙醇含量(P<0.05～0.01).结论本品具有较好预防醉酒和解酒作用,其作用机理可能与其降低血中乙醇含量有关.     

解酒保肝剂对小鼠酒精中毒的影响

目的 观察解酒保肝剂对小鼠醉酒实验、血清乙醇浓度和肝组织丙二醛含量的影响。方法 50只小鼠随机分为给药组和对照组,每组25只。给药组小鼠给予解酒保肝剂灌胃,对照组给予双蒸馏水灌胃。记录小鼠翻正反射消失及恢复时间,取肝匀浆,检测肝脏丙二醛(MDA)含量,用顶空气相色谱法检测血酒精浓度。结果 与对照组比较,给药组翻正反射消失时间明显延长(P<0.01),翻正反射时间明显缩短(P<0.05),肝MDA含量显著降低(P<0.05),血酒精含量显著降低(P<0.01)。结论 解酒保肝剂具有良好的解酒作用。     

醒酒护肝口服液的安全性评价及抗醉、解酒作用的研究

目的考察醒酒护肝VI服液的安全性并评价其抗醉、解酒作用。方法醒酒护肝口服液以最大浓度、最大给药剂量灌胃小鼠,观察24h内动物急性毒性反应及死亡情况,并继续观察14d以评价其安全性,同时计算小鼠最大耐受剂量;建立小鼠酒精致醉模型,以自主活动数、翻正反应消失时间及恢复时间评价醒酒护肝口服液抗醉、解酒作用。结果醒酒护肝口服液小鼠最大给药剂量为350．0g/kg,在24h内未见实验动物急性毒性反应和死亡,14d实验周期内,小鼠体质量呈进行性增长,肝功能指标未见异常;抗醉实验中,醒酒护肝口服液能显著降低致醉小鼠自主活动次数、延长醉酒时间并缩短醉睡时间：解酒实验中．醒酒护肝口服液提高醉酒时间、醉睡时间。结论醒酒护肝口服液临床剂量是合理安全的,对酒精致醉模型小鼠有抗醉作用。     

加味醒酒汤解酒作用的研究

目的 研究加味醒酒汤对醉酒小鼠的解酒作用。方法 根据建立的小鼠醉酒模型,通过测定小鼠醉酒潜伏期与醒酒时间,确定加味醒酒汤的最佳工艺;通过测定小鼠血液乙醇浓度的含量及肝脏乙醇代谢酶的活性来观察加味醒酒汤的解酒效果。结果 加味醒酒汤能够增加小鼠对酒精的耐受时间,同时缩短小鼠的醒酒时间,降低血液中的乙醇浓度,提高肝脏中ADH、ALDH与GSH-Px的活性。结论 加味醒酒汤对醉酒小鼠具有解酒作用,其机制可能与提高乙醇代谢酶的活性有关。     

大籽獐牙菜醇提物解酒保肝作用的实验研究

目的：对大籽獐牙菜乙醇提取物在解酒保肝方面的作用进行初步研究探讨。方法采用纠正运动失调作用实验、解酒实验和预防醉酒实验,同时测定急性酒精性肝损伤小鼠的血清丙氨酸转换酶（ALT）和肝糖原的含量。结果大籽獐牙菜醇提取物可显著延长小鼠酒后在网停留时间;使给药组的翻正反射恢复时间较对照组显著缩短;给药后醉酒小鼠数较未给药组显著减少;可对抗乙醇对小鼠肝脏造成的损伤,使谷丙转氨酶活力显著下降,促进肝糖原的分解,对抗乙醇造成的低血糖。结论大籽獐牙菜提取物具有纠正运动失调、解酒以及预防酒醉作用,其对乙醇所致的肝损伤有防治作用。     

解酒饮的药理学研究

目的:研究解酒饮的解酒作用.方法:40只小鼠随机分成空白对照组,胆维他对照组(25mg·g-1)和高低剂量解酒饮组(25,12.5g·kg-1).用自制30%白酒按14mL·kg-1灌胃造成小白鼠醉酒模型,分别在造模前后单次给药,观察小白鼠翻正反射消失的时间和小鼠酒醉持续时间.结果:与空白对照组比较,解酒饮25g·kg-1组小鼠翻正反射消失时间显著延长,酒醉持续时间显著缩短.而解酒饮12.5g·kg-1组无显著性差异.结论:按生药25g·kg-1给予解酒饮,对于小白鼠具有预防醉酒和醒酒的作用.     

赶黄草对预防醉酒及解酒效能研究

目的研究赶黄草的预防醉酒和解酒作用。方法通过五粮春造成小白鼠醉酒的模型,再分别按试验组给予一定剂量的赶黄草、郁金、生理盐水,观察其醒酒时间,翻正反射。结果赶黄草组与生理盐水组比较,小鼠翻正反射消失时间和酒醒时间有显著性差异。而郁金组与生理盐水组比较,小鼠翻正反射消失时间和酒醒时间无显著性差异。     

Disulfiram enhances ethanol pharmacological activity and impairs its elimination

Disulfiram or diethyldithiocarbamate (DDC) significantly prolonged ethanol-induced loss of righting reflex in mice. The disappearance of ethanol from blood, and brain was significantly delayed in disulfiram-treated animals, suggesting an impairment in the activity of alcohol dehydrogenase in these animals. DDC, an active metabolite of disulfiram, inhibited mouse liver alcohol dehydrogenase (LADH) in vitro. Pyrazole, a known inhibitor of alcohol dehydrogenase, affected ethanol elimination and ethanol-induced loss of righting reflex in mice in a manner similar to that seen with disulfiram.     

Non-specific prolongation of the effects of general depressants by pyrazole and 4-methylpyrazole

The liver alcohol dehydrogenase inhibitors, pyrazole and 4-methylpyrazole, have been tested for their ability to prolong drug-induced sleep times in mice. Both drugs (at 1 mmol kg-1 i.p.) prolonged the duration of loss of righting reflex following chloral hydrate, pentobarbitone, barbitone, temazepam and halothane, but not diethyl ether. This suggests that the effects of these pyrazoles are not specific to the inhibition of liver alcohol dehydrogenase.     

Inhibition of alcohol dehydrogenase by dimethyl formamide and dimethyl sulfoxide

Dimethyl formamide (DMF) and dimethyl sulfoxide (DMSO) inhibit mouse liver alcohol dehydrogenase (LADH) in vitro. The inhibition is “uncompetitive” with both DMF and DMSO, where both Km and Vmax were changed in the presence of the inhibitor. Both DMF and DMSO prolonged significantly ethanol-induced loss of righting reflex in mice, but not barbital-induced loss of righting reflex.     

Pharmacological and metabolic interactions between ethanol and the dopamine-β-hydroxylase inhibitor FLA 63 in mice

The duration of ethanol-induced loss of righting reflex was significantly prolonged in mice pretreated with the dopamine-β-hydroxylase inhibitor FLA 63. The disappearance of ethanol from blood, brain, liver and kidneys from FLA 63-treated mice was significantly delayed as compared to control mice. In vitro, FLA 63 inhibited the activity of mouse liver alcohol dehydrogenase. These results demonstrate that FLA 63 can alter the disposition of ethanol. Consequently, its pharmacological activity is altered. The interpretation of results from experiments in which FLA 63 is employed with other drugs should not be based solely on its inhibitory action on dopamine-β-hydroxylase.     

Inhibition of mouse liver alcohol dehydrogenase by methyl N-butyl ketone

Methyl N-butyl ketone (MNBK) inhibited the activity of mouse liver alcohol dehydrogenase (LADH) in vitro. Ethanol elimination was reduced in MNBK-treated mice as compared to controls. Ethanol-induced induced loss of righting reflex was significantly prolonged in mice pretreated with MNBK.     

Acute tolerance in inbred and selected lines of mice

Mice of the C57Bl and C3H strains regained their righting reflex at higher brain ethanol levels than those at which they had lost their righting reflex, indicating that these animals developed acute tolerance. DBA mice did not develop acute tolerance. DBA mice "slept" significantly longer than C57Bl mice, but all mice lost their righting reflex at similar brain ethanol levels. Mice of SS and LS lines also showed no evidence for developing acute tolerance but differed significantly in brain ethanol levels upon loss of righting reflex. Both acute tolerance development and initial brain sensitivity to ethanol seem to determine duration of ethanol "sleep time" in mice.     

Effects of cyanamide and acetaldehyde accumulation on the locomotor stimulant and sedative effects of ethanol in mice

Ethanol administration induces both locomotor stimulant and sedative effects depending upon blood ethanol concentrations. Recent studies in rats and mice suggest that acetaldehyde, the first product of ethanol metabolism, might be involved in the expression of both the stimulant and the sedative effects of ethanol. A number of studies have used the drug cyanamide in an attempt to clarify the role of acetaldehyde in the behavioral effects of ethanol. The results of such studies are, however, difficult to interpret because cyanamide is an inhibitor of the enzymes catalase and aldehyde dehydrogenase, two enzymes with opposite effects on brain acetaldehyde concentrations. This study was aimed at clarifying the effects of cyanamide on ethanol-induced locomotor stimulant and sedative effects in Swiss mice. The locomotor stimulant effects of ethanol were measured in standard activity boxes, whereas the sedative effects of ethanol were quantified using the loss of righting reflex procedure. Cyanamide prevented the locomotor stimulant effects of 2 g/kg ethanol, although this was mainly due to a potentiation of the inhibitory effects of ethanol as evidenced by a prolongation of ethanol-induced loss of righting reflex. Additionally, 4-methylpyrazole, an inhibitor of the enzyme alcohol dehydrogenase, prevented these effects of cyanamide. It is concluded that in vivo the effects of cyanamide are predominantly due to the inhibition of the enzyme aldehyde dehydrogenase, rather than to its effects on catalase.     

Pharmacological and Metabolic Interactions between Ethanol and Methyl n-Butyl Ketone, Methyl Isobutyl Ketone, Methyl Ethyl Ketone, or Acetone in Mice

Methyl n-butyl ketone (MnBK), methyl isobutyl ketone (MIBK),methyl ethyl ketone (MEK), and acetone are widely used industrialsolvents to which certain groups of workers are exposed. Pharmacologicaland metabolic interactions between these solvents and ethanolwere explored in male CD-1 mice. The effects of these solventson the duration of ethanol-induced loss of righting reflex andon ethanol elimination in mice were studied. The solvents weredissolved in corn oil and injected intraperitoneally 30 mm beforeethanol 4 g/kg ip. The four solvents prolonged significantlythe duration of ethanol-induced loss of righting reflex whengiven in the following doses (m mol/kg): MnBK, 3.75 and 5; MIBK,5; MEK, 5 and 10, acetone, 20 and 40. This prolongation wasdose related and increased as the dose of the solvent was increased.The concentrations of ethanol in blood or brain on return ofthe righting reflex were similar in solvent-treated and controlanimals, with the exception of the group of mice treated with40 mmol/kg acetone in which the ethanol concentrations weresignificantly lower than in control animals. The mean eliminationrate of ethanol was markedly reduced in mice treated with MnBK5 mmol/kg, MEK 15 mmol/ kg, and acetone 40 mmol/kg. All foursolvents reduced the activity of mouse liver alcohol dehy-drogenasein vitro. It is concluded that enhancement of the ethanol-inducedloss of righting reflex by these solvents in mice is well correlatedto reduced elimination rate of ethanol.