叠氮化钠所致大鼠中枢神经系统的病理改变

２４只雄性大鼠以３ｍｇ／ｋｇ叠氮化钠作腹腔注射，染毒，每日６次，每次间隔０．５ｈ，连续４ｄ直至中毒。神经病理检查结果表明，叠氮化钠对脑的损伤呈双侧对称性，主要是尾－壳核。光镜下可见神经元胞浆深染，核固缩，神经纤维束疏松肿胀，重者呈网眼状。电镜下早期可见神经元胞浆疏松，继而固缩，核染色质积聚，细胞周围可见肿胀的突起。神经纤维、胶质细胞和血管也出现病变。同时用大鼠建立了一个叠氮化钠引起脑内尾－壳核损伤的动物模型，以用于中毒机理研究。     

Is delayed neurotoxicity a property of all organophosphorus compounds? A study with a model compound: Parathion

A recently reported hypothesis of other investigators that the induction of delayed neurotoxicity is a property of all organophosphorus compounds including parathion was evaluated in light of the inability of parathion to induce in our laboratory any clinical, histological, or biochemical signs of delayed neurotoxicity in hens following a very sensitive dosing regimen. Parathion was administered orally or applied dermally as 1 mg/kg/day for 1 week and then the dose was increased by 1 mg/kg/day at weekly intervals up to 6 mg/kg/day which was given thereafter until a total of 90 doses. Results indicate that parathion either orally or dermally did not produce delayed neurotoxicity in hens comparable to that induced by tri-ortho-cresyl phosphate (TOCP) in this experiment. This finding is supported by clinical, histological, and biochemical evidences. No clinical signs or histopathological changes in spinal cords and sciatic nerves of the type associated with delayed neurotoxicity were observed in any of the surviving parathion- treated hens. Moreover, this existence treatment with parathion resulted in no significant in vivo effect on neurotoxic esterase, an esterase believed to be the initial target in the genesis of delayed neurotoxicity. These results agree with the general hypothesis that delayed neurotoxicity is a special toxic effect of some but not all of the organophosphorus esters.     

Muscle spindle function in organophosphorus neuropathy

The contribution of muscle spindle dysfunction to the neurological signs odelayed organophophorus neuropathy was investigated in the hindlimbs of cats intraf arterially injected with 2 mg/kg of diisopropylfluorophosphate (DFP). In this model of a delayed peripheral neuropathy, the animals exhibit a peculiar high-step gait and a sluggish response to noxious stimuli. These signs initially appear 14 days and are maximum 21–28 days after DFP administration. The position sensitives of secondary but not primary soleus muscle spindles were depressed at 14 days after DFP.At 21 days after DFP, both primary and secondary endings had attenuated position sensitivities and significantly elevated thresholds. Spindle functions was normal at 56 days after DFP exposure. The onset, peak and recovery of soleus muscle spindle dysfunction corresponded to those in α-motor axons, indicating the mixed sensory motor nature of organophophorus neuropathy. Thus impairment of both sensory and motor functions contributes to the neurological signs of this neuropathy.     

Impact of paracetamol pack size restrictions on poisoning from paracetamol in England and Wales: an observational study

BACKGROUND: About 500 drug poisoning deaths involving paracetamol (acetaminophen) occur every year in England and Wales. To reduce the number of deaths, regulations were introduced in 1998 to restrict the sale of paracetamol. In this paper, we evaluate the impact of these regulations. METHODS: Mortality data for England and Wales were provided by the Office for National Statistics. Deaths were defined as due to compound paracetamol (paracetamol in combination with another analgesic, a low dose opioid or other ingredients) or paracetamol only, with or without alcohol or other drugs. The Department of Health provided data on all hospital admissions with a primary diagnosis of paracetamol poisoning. RESULTS: Mortality rates for paracetamol only were similar for males and females, and decreased from about 4.5 to 2.8 per million between 1997 and 1999 and again from about 3.1 to 2.2 per million between 2001 and 2002. These falls may be attributable to random variation in the rates. Deaths involving compound paracetamol, which were not subject to the 1998 regulations, remained relatively constant over the study period. There was evidence of a decreasing trend in paracetamol only mortality rates and this followed overall trends for other drug poisoning excluding opioids and drugs of misuse. Hospital admissions due to paracetamol poisoning increased from about 27 000 to 33 000 between 1995/1996 and 1997/1998 and then decreased to 25 000 in 2001/2002. There were almost 50 per cent more admissions for females than males, with the highest admission rates amongst females aged 15-24 years old. CONCLUSIONS: Between 1993 and 2002, mortality rates and hospital admissions due to paracetamol poisoning declined. However, the contribution of the 1998 regulations to this decline is not clear. Paracetamol poisoning continues to be an important public health issue in England and Wales and represents significant workload for the NHS in England.     

PICU中毒患儿相关因素分析及干预

目的探讨PICU收治的儿童中毒病例的相关因素以寻求相应的防治措施。方法回顾性分析2008年1月-2010年12月首都医科大学附属北京儿童医院PICU救治的127例(<18岁)中毒患儿病例资料,分为药物中毒组和非药物中毒组,分析2组不同特点。结果 7月是中毒高发月份。儿童中毒主要发生在家中,其中农村中毒发生率较城市高。所有中毒患儿中,意外中毒105例,1～3岁是意外中毒发生的主要年龄段,且男童发生率高。非意外中毒22例中,以学龄期和青春期为主要年龄段。药物中毒儿童66例,毒物以神经系统治疗药物为首,其次为精神障碍治疗药物,中毒症状以神经系统症状为首。非药物中毒儿童61例,毒物以杀虫(鼠)剂为首,中毒症状以消化系统症状为首。2组呼吸机治疗时间比较差异无统计学意义(Z=-0.183,P=0.931),血液净化治疗时间比较差异有统计学意义(Z=-3.762,P=0.000)。药物中毒组和非药物中毒组治愈好转率比较差异无统计学意义。药物中毒组住院时间较非药物中毒住院时间短(t=2.326,P=0.024)。结论血液净化是儿童中毒救治的重要手段,呼吸支持为急性中毒患儿最终的治疗成功提供了保证。儿童中毒应以预防为主。     

Leading causes of injury hospitalisation in children aged 0–4 years in New South Wales by injury submechanism: A brief profile by age and sex

Aim: To identify the leading causes of injury in children aged 0–4 years by single year of age using injury submechanisms and present a brief epidemiologic profile of each cause. Methods: Hospitalisation data for New South Wales from 1999 to 2009 were used to identify the leading causes of injury for children aged 0–4 years by single year of age. For each leading cause, rates over time and by sex were calculated by single year of age. Associated age and sex risk ratios were estimated. Results: The leading causes of injury for children aged <1, 1 and 2 years were falls while being carried, burns by hot non‐aqueous substances and poisoning by other and unspecified pharmaceutical substances, respectively. Falls involving playground equipment ranked first for children aged 3–4 years. Each leading injury cause exhibited an age pattern that remained stable over time and by sex. Age predicted falls while being carried and both age and sex predicted the remaining leading injury causes, with age and sex interacting to predict burns by hot non‐aqueous substances. Conclusions: Epidemiologic analysis using single‐year age intervals and injury submechanisms results in a clearer picture of injury risk for young children. The findings of this study provide detailed information regarding the leading causes of hospitalised injury in young children by age and sex. Child health‐care providers can use this information to focus discussions of child development and injury risk with families of young children and suggest appropriate prevention measures in terms of a child's age and sex.     

中毒所致的发作性睡病

目的 加强对中毒所致的发作性睡病的认识.方法 对2例中毒后出现发作性睡病患者的临床资料进行分析,并对一些相关文献进行复习.结果 发作性睡病包括原发性及继发性,中毒所致的发作性睡病属继发性.白天发作性嗜睡、猝倒、睡眠瘫痪以及睡眠幻觉是该病的4个主要症状.发作性睡病与病理性REM睡眠相关.结论 中毒也可能导致发作性睡病,但可能不被识别而被误诊为其他疾病,有必要加强对发作性睡病以及REM睡眠的认识.     

急性百草枯中毒患者入院时百草枯血药浓度与肺泡灌洗液中内皮素-1浓度的关系

目的探讨急性百草枯中毒患者百草枯血药浓度与患者肺泡灌洗液中内皮素-1(ET-1)的关系。方法百草枯中毒患者15人(观察组),按照患者入院时血药浓度又分为0～4 mg.L-1组、4～8 mg.L-1组、8～12 mg.L-1组、>12 mg.L-1组,对照组为健康体检者10人,采用酶联免疫吸附法测所有研究对象肺泡灌洗液中ET-1的浓度。结果观察组ET-1浓度(31.40±8.12)μg.L-1高于对照组(18.71±6.89)μg.L-1(P<0.05);ET-1的浓度随中毒剂量的升高而升高(P<0.05)。结论百草枯中毒患者肺泡灌洗液中ET-1水平可判断患者病情的重要指标之一。