急性乙醇中毒合并急性敌敌畏中毒的临床特点

目的探讨急性乙醇中毒合并敌敌畏中毒时,血浆中乙醇浓度与血浆中敌敌畏含量及患者预后的相关性。方法将74例敌敌畏中毒患者分为单纯中毒组与混合中毒组,所有患者均检测其入院时血浆中胆碱酯酶、敌敌畏浓度,对合并乙醇中毒者检测血浆中乙醇浓度,对两组患者的性别、年龄、敌敌畏浓度、胆碱酯酶活力和死亡率进行统计学分析,并对乙醇浓度与敌敌畏浓度及胆碱酯酶活力进行相关分析。结果与对照组相比,混合中毒组男性患者明显高于女性,其血浆中敌敌畏浓度、患者病死率明显升高,胆碱酯酶活力降低显著;血浆中乙醇浓度与血浆中敌敌畏浓度呈正相关,而与胆碱酯酶活力呈负相关;结论急性乙醇中毒合并敌敌畏中毒时,血浆敌敌畏浓度明显升高,病死率明显增加。     

酒类食黾对小鼠神经功能的影响

目的观察不同剂量的乙醇、甲醇对小鼠神经功能的影响。方法用急性灌胃的方法染毒小鼠,实验分三组,即甲醇染毒组、乙醇染毒组、甲醇与乙醇组,采用爬杆实验装置测定小鼠神经功能,用秒表测定小鼠染毒前后的爬杆时间,分析各组间及组内处理爬杆时间的差异。结果小鼠爬杆时间随乙醇、甲醇染毒的剂量增大而减少,呈明显的剂量-效应关系,经统计分析显示,差异有显著性。结论甲醇与乙醇影响小鼠的爬杆时间,具有神经毒性。     

1,6-二磷酸果糖对急性一氧化碳中毒致小鼠脑损伤的治疗作用

目的 研究1，6-二磷酸果糖(FDP)对急性一氧化碳(CO)中毒致小鼠脑损伤的治疗作用。方法 小鼠单次腹腔注射CO170ml／kg，以CO中毒小鼠死亡率，被动回避性记忆能力、脑细胞膜和线粒体膜Ca^2 Mg^2 -ATPase活力、脑组织单氨氧化酶B(MAO-B)活力、海马病理形态学的改变为指标，研究FDP对急性CO中毒致小鼠脑损伤的治疗作用。结果 FDP以剂量依赖性的方式降低CO中毒小鼠的死亡率，明显改善CO中毒小鼠记忆能力的下降，显著阻遏CO中毒小鼠脑细胞膜和线粒体膜Ca^2 Mg^2 -ATPase活力的病理性降低以及脑组织MAO-B活力的病理性升高，并能一定程度避免海马神经元损。此治疗作用以CO中毒15min内给予FDP最为明显。结论 在急性CO中毒后早期给予足量FDP对急性CO中毒所致脑损伤有显著的治疗作用。     

48例急性乙醇中毒昏迷期患者诊断抢救疗效的回顾性分析

目的探究48例急性乙醇中毒昏迷期患者诊断抢救疗效。方法对48例急性乙醇中毒昏迷期患者给予洗胃、导泻处理,纳洛酮促醒、呼吸机抢救措施,观察临床疗效。结果总有效率为91.67%。44例抢救成功的急性乙醇中毒昏迷期患者,首次清醒时间均在2h以内,完全清醒时间均在2-4h以内。呼吸恢复时间为55.2±10.3min,血压恢复时间为24.6±4.8min,体温恢复80.5±10.3min。结论对急性乙醇中毒昏迷期患者实施积极的抢救措施,有利于促进患者苏醒,降低死亡率。     

尼莫地平对急性一氧化碳中毒小鼠脑损伤的治疗作用

目的 研究尼莫地平对急性一氧化碳（CO）中毒致小鼠脑损伤的治疗作用。方法 小鼠单次腹腔注射CO170ml/kg，以CO中毒小鼠死亡率，被动回避性记忆能力，脑细胞膜和线粒体膜Ca^2 -Mg^2 ATP酶（Ca^2 -Mg^2 ATPase)活性和脑组织单腔氧化酶-B（MAO-B）活性的改变以及海马神经元细胞病理改变为指标，研究尼莫地平对急性CO中毒致小鼠脑损伤的治疗作用。结果 尼莫地平以剂量依赖性的方式变为指标。研究尼莫地平对急性CO中毒致小鼠脑损伤的治疗作用。结果 尼莫地平以剂量依赖性的方式降低CO中毒小鼠的死亡率，明显改善CO中毒小鼠下降的记忆能力。显著阻遏CO中毒小鼠脑细胞膜和线粒体膜Ca^2 -Mg^2 ATPase活性的病理性降低以及脑组织MAO-B活性的病理性升高，明显减轻海马神经元的迟发性坏死；此治疗作用以尼莫地平15min内给予较为明显。结论 在急性CO中毒早期给予足量尼莫地平对急性CO中毒所致脑损伤有显著的治疗作用。     

γ-羟基丁酸与二巯丙磺酸钠对急性毒鼠强中毒小鼠的治疗作用

目的 探讨γ-羟基丁酸与二巯丙磺酸钠对急性毒鼠强中毒小鼠的疗效.方法 对小鼠用一次性口服毒鼠强染毒(每10 g体重0.025 mg毒鼠强)后将60只小鼠分为对照组、治疗1组、治疗2组和治疗3组,每组15只.治疗1组给予二巯丙磺酸钠(每10 g体重注射2.5 mg剂量)、治疗2组给予γ-羟基丁酸(每10 g体重注射1.25 mg剂量)、治疗3组的γ-羟基丁酸+二巯丙磺酸钠腹腔注射,观察各组小鼠发生中毒惊厥潜伏期、1 h内抽搐间隔时间、平均死亡时间、死亡小鼠数和死亡率.结果 治疗1组1 h死亡率与对照组比较,差异有统计学意义(P＜0.05);治疗2组和治疗3组1、24 h死亡率明显低于对照组及治疗1组,差异有统计学意义(P＜0.05);治疗2组和治疗3组中毒惊厥潜伏期分别为(9.6±3.5)、(10.7±3.9)min,1 h内抽搐间隔时间分别为(11.8±4.0)、(12.1±5.1)min,平均死亡时间分别为(58.7±17.6)、(67.7±18.6)min,比对照组和治疗1组延长,差异均有统计学意义(P＜0.05).而治疗1组中毒惊厥潜伏期、1 h内抽搐间隔时间及平均死亡时间与对照组比较,差异均无统计学意义(P＞0.05).结论 二巯丙磺酸钠对急性毒鼠强中毒小鼠无肯定的治疗作用,γ-羟基丁酸能明显延缓小鼠中毒后的惊厥、抽搐发作,降低死亡率.     

肉苁蓉茶对小鼠抗疲劳和耐缺氧能力的影响

[目的]研究肉苁蓉茶对小鼠抗疲劳和耐缺氧能力的影响。[方法]分别以3333、1667、833mg/kgBW剂量(以茶颗粒干品计)的肉苁蓉茶提取液,给小鼠连续灌胃35d,通过负重游泳试验、尿素氮和肝糖原测定评价其抗疲劳功能,通过常压耐缺氧试验、亚硝酸钠中毒试验和急性脑缺血(断头)试验评价其耐缺氧功能。[结果]在本实验条件下,肉苁蓉茶能够延长小鼠的负重游泳时间,增加小鼠的肝糖原的储备量,减小小鼠运动后的血乳酸量,对疲劳小鼠的血清尿素氮无明显影响;肉苁蓉茶能够延长小鼠在常压下缺氧存活时间及硝酸钠中毒后的存活时间,对急性脑缺血(断头)后张口喘气时间无明显影响。[结论]肉苁蓉茶可以提高小鼠的抗疲劳能力和常压耐缺氧能力。     

尼莫地平对一氧化碳中毒致小鼠脑损伤保护作用研究

小鼠腹腔注射CO100ml/kg,每天1次,连续7天,尼莫地平（Nimodipine）1mg/kg在每次给予CO前30发钟腹腔注射。停止给预CO后,以CO中毒小鼠死亡率,被动回避性学习记忆能力改变,脑组织病理学和单胺氧化酶－B活性改变为指标观察尼莫地平对一氧化碳中毒致小鼠迟发性脑损伤保护作用。结果显示,给预尼莫地平能显著降低CO中毒死亡率;基本逆转小鼠CO中毒引起的学习记忆能力的损害;能防止海马神经元细胞延迟性死亡;并能阻遏CO中毒引起的小鼠脑组织单胺氧化酶－B活性的病理性升高。提示,尼莫地平对一氧化碳中致小鼠迟发生脑损伤有明显的保护作用。     

生川乌对小鼠神经行为的影响

[目的]研究生川乌对小鼠记忆获得能力、肌耐力和自发活动3种神经行为的影响.[方法]选用神经行为测试组合即Morris水迷宫试验、爬杆试验及小鼠自发活动试验,分别观察小鼠平均逃避潜伏期、爬杆持续时闻、小鼠自发活动数,每个试验设27.6、13.8、6.9g生药/kg 3个剂量组、阴性对照组和阳性对照组.[结果]在Morris水述宫试验中高剂量组小鼠平均逃避潜伏期与阴性对照组相比,差异有统计学意义(P<0.05),其余剂量组小鼠平均逃避潜伏期与阴性对照组比较,差异均无统计学意义(P>0.05);爬杆试验中,各剂量组爬杆持续时间与对照组相比无统计学意义(P>0.05);在小鼠自发活动试验中,高剂量组小鼠在给药后30min自发活动数明显低于阴性对照组,差异有统计学意义(P<0.05),而中、低剂量组与阴性对照组相比,小鼠自发活动数的差异无统计学意义(P>0.05).[结论]在本实验条件下,尽管生川乌对小鼠的肌耐力无明显影响,但27.6g生药/kg体重时,可影响小鼠记忆获得能力以及抑制小鼠的自发活动,所以生川乌对小鼠神经行为仍有不良影响.     

三康胶囊抗疲劳作用与血液生化指标的改变

目的探讨三康胶囊(SKC)抗疲劳作用与血液生化指标改变的关系。方法灌胃给予高、低剂量的SKC,(1.5g/kg、0.5g/kg),采用小鼠疲劳爬杆实验评价药物的抗疲劳效果。同时,观察游泳疲劳状态下相关的代谢产物如血乳酸、血尿素氮含量的变化。结果与爬杆对照组相比,SKC高、低剂量组分别延长爬杆时间42.98%(P<0.05)和14.77%;SKC还可升高外周血红细胞数和血红蛋白含量。与游泳模型组相比,SKC高剂量组可增加疲劳状态下血浆中乳酸脱氢酶(LDH)活性(6.62±0.37vs6.08±0.38,P<0.05),减少血乳酸含量(9.45±1.38vs11.68±1.20,P<0.05),降低长时间运动后升高的血尿素氮(13.24±1.86vs16.51±2.14,P<0.05)。结论SKC具有抗疲劳的作用,其机制可能与血液生化指标的改善有关。     

Effect of acute alcohol intoxication on the opioid system in humans

We investigated the possible relation between the endogenous opioid system and acute alcoholic intoxication in 21 subjects, of whom 13 were drinkers who came to the emergency service with evident symptoms of drunkenness, and 8 were nondrinkers who consumed 1 g alcohol per kg body weight over a short period. Different patterns of changes were found in the two groups for plasma concentrations of β-endorphin and adrenocorticotropic hormone. In drinkers, plasma levels of both substances increased, whereas in nondrinkers both concentrations decreased, the declines being especially notable 15, 30, and 45 min after ingestion. We found no differences between the two groups in plasma cortisol concentrations. The different levels of these substances may reflect differences in drinking behavior between the two groups.     

Jejunal uptake of thiamin hydrochloride in man: influence of alcoholism and alcohol

The jejunal uptake of 35S-thiamin hydrochloride was examined using an intestinal perfusion technique in six young students (group 1), 12 recently drinking alcoholic men (group 3) and in 6 non-drinking men age-matched with the alcoholic men (group 2). The acute effect of alcohol on thiamin uptake was also examined in the alcoholic subjects. At a perfusate thiamin concentration of 0.5 mumol/l, median thiamin uptake was 34.4, 10.4, and 6.8 ng/cm/min in groups 1, 2, and 3 respectively, while for 8.0 mumol thiamin/l, median uptake was 277.2, 102.3, and 98.0 ng/cm/min for these groups respectively. Alcohol, 50 g/l, added to the perfusate gave a 28.9% decrease in uptake of 0.5 microM thiamin, which was not statistically significant. These findings suggest that neither alcoholism nor acute exposure to alcohol limits jejunal uptake of thiamin hydrochloride. Differences noted between young and old controls need further study.     

ALCOHOL INTOXICATION IN CHILDHOOD AND ADOLESCENCE

Coma and vomiting are the commonest symptoms in young teenagersintoxicated by alcohol. Severe toxicity, manifested as coma,occurs at lower blood alcohol concentrations in young teenagersthan in adults. The effect of ethanol on the state of consciousnessis directly proportional to blood alcohol concentration. Amongchildren under 5 years of age the risk of hypoglycaemia is increased.A significant risk in acute alcohol intoxication is the rapiddevelopment of coma, which in cold environments could lead tofatal hypothermia. Preschool-age children are reported to eliminateethanol twice as fast as adults, whereas young teenagers eliminateit at the adult rate. The biochemical disturbances in children11 to 16 years of age with alcohol intoxication resemble thoseof adults. Mild acidosis of a respiratory or metabolic originand mild hypokalaemia are common findings in young teenagers.Fluid replacement with glucose-containing fluids and follow-upare generally the only treatments needed for complete recovery.Motives leading to alcohol intoxication are a wish to get drunk,experimenting, problems in human relations, and attempted suicide.The underlying problems are often family-related. such as divorce,an alcoholic parent and a lower socioeconomic group.     

纳美芬和纳洛酮对急性重度乙醇中毒疗效比较

目的：探讨纳美芬和纳洛酮对急性重度乙醇中毒的疗效,为临床用药提供参考。方法：将2012年1月-2013年12月我院急诊科收治急性重度乙醇中毒患者110例,分为两组,治疗组和对照组各55例,治疗组在常规治疗基础上给予盐酸纳美芬治疗;对照组在常规治疗基础上给予纳洛酮治疗,观察并比较两组患者观察患者治疗后30分、60分钟、90分钟和150分钟神志意识恢复情况。结果：总有效率和显效率比较,治疗后30分钟、60分钟、90分钟和150分钟治疗组均优于对照组。结论：纳美芬对急性重度乙醇中毒患者进行治疗相比纳洛酮具有更为显著的临床疗效,能够明显加快药效起作用时间,减少症状的缓解和消退时间,具有且不良反应少特点,可以在基层临床上推广应用。     

Biochemical Mechanisms of the Alcohol-Induced Liver Injury

1. The biochemical mechanisms of the alcohol-induced liver injuryare reviewed. 2. Acute alcohol intake causes redox changes inpyridine nucleotides, a fatty liver and an exacerbation of hepaticporphyrias. 3. The redox changes are caused by alcohol metabolism,and it is hoped that substances other than fructose, which areknown to accelerate alcohol metabolism, will be tested clinicallyin acute alcoholic intoxication. 4. The acute fatty liver isproduced by an increased hepatic uptake of plasma free fattyacids secondary to enhanced hepatic blood flow, an activationof phosphatidate phosphohydrolase and a possible hypermobilizationof adipose-tissue fat. 5. The alcohol exacerbation of hepaticporphyrias may be due to the further removal of the regulatoryhaem pool controlling haem biosynthesis. 6. Chronic alcoholintake causes redox changes similar to those mentioned above,a fatty liver and hepatitis, cirrhosis and necrosis. 7. Theredox change in the NADP couple is caused by that in the NADcouple. 8. The chronic fatty liver is produced mainly by anincreased esterification of fatty acids. Dietary fat plays animportant role, and factors such as increased hepatic uptakeof plasma free fatty acids and activation of phosphohydrolasemay also be involved. 9. We know very little about the biochemicalpathology of the alcoholic hepatitis and cirrhosis. 10. In experimentalanimals, chronic alcohol consumption causes hepatic-cell necrosisif the liver is either exposed to a high concentration of alcoholor if made anoxic by exposing the animals to low oxygen atmospheresor by bleeding. 11. There is evidence that acetaldehyde maybe involved in some of the hepatotoxic effects of alcohol. 12.Alcohol also causes lipid peroxidation and the possibility thatdestruction of membrane phospholipid is involved in the hepatotoxicityof alcohol cannot be ruled out.     

Alcohol intoxication and alcoholism in acute male medical admissions

In order to assess alcohol related morbidity in male hospital patients we studied all acute male admissions over a period of three months. 9.3% of patients were found to have detectable alcohol on admission (level greater than 4 mmol/l). A total of 28.3% of admissions were judged to be alcoholic by questionnaire (Michigan Alcohol Screening Test). These results suggest that acute intoxication in male hospital admissions is not as common as previously recorded. The prevalence of alcoholism, however, was disturbingly high and has significant implications for in-patient management.     

急性酒精性肝损伤与肝细胞凋亡的研究

目的研究急性酒精性肝损伤肝细胞凋亡,探讨其发病机制。方法将30只大鼠随机分成酒精组(20只),对照组(10只)。给酒精组大鼠按体重15 g/kg 47.5%酒精一次性灌胃,给对照组大鼠按体重15 g/kg生理盐水一次性灌胃。灌胃后48 h处死大鼠,用光镜、TUNEL、电镜检查肝组织。结果酒精组肝损伤、肝细胞凋亡检出率均为100%,凋亡肝细胞核数占肝细胞核总数的46.8%。生理盐水组未发现肝损伤病变,仅3例个别视野近肝小叶中央静脉处见单个凋亡细胞。结论肝细胞凋亡与急性酒精性肝损伤有一定的关系。     

姜精油对小鼠急性酒精性肝损伤的辅助保护作用

目的研究姜精油对小鼠急性酒精性肝损伤是否具有辅助保护作用。方法将70只BALB/C小鼠随机分为空白对照组,急性酒精性肝损伤模型组,姜精油超低剂量组(62.5mg/kg)、极低剂量组(125mg/kg)、低剂量组(250mg/kg)、中剂量组(500mg/kg)和高剂量组(1000mg/kg)7组,每组10只。常规喂养,每日灌胃给药1次,连续给药30天,第31天采用50%无水乙醇溶液进行一次性灌胃后断头处死。检测各组小鼠肝匀浆中的甘油三酯(TG)、丙二醛(MDA)和谷胱甘肽(GSH)水平,并进行肝脏病理组织学检查。结果随姜精油剂量的增加,小鼠肝组织匀浆的中TG值呈下降趋势,其中中剂量组和高剂量组与急性酒精性肝损伤模型组间存在显著差异(P<0.05);各剂量组的MDA值均明显低于急性酒精性肝损伤模型组(P<0.01),其中低剂量组的MDA值最低;极低剂量组和低剂量组的GSH值明显高于急性酒精性肝损伤模型组(P<0.05,P<0.01);低剂量组、中剂量组和高剂量组的肝脏病理组织检查评分明显低于急性酒精性肝损伤模型组(P<0.01)。结论姜精油对酒精性肝损伤具有辅助保护作用。     

Analysis of mortality rate as a result of alcoholic poisoning

The indices of mortality due to intoxication by alcohol and its surrogates in a region studied during the 90-ies essentially differ depending on an information source. An analysis of the alcoholic situation in the region and en elaboration of preventive measures cannot be limited to data on the consumption of alcohol (provided by the State Statistics Committee) showing only the volume of statistically registered sales of alcoholic beverages through the trade network. If this factor is ignored, erroneous conclusions can be made on both the volumes of average-per-capita consumption of alcohol and on the reasons of changes in people's health indices.