燃煤污染型氟中毒大鼠学习记忆能力及胆碱酯酶活性改变

目的 观察燃煤污染型氟中毒大鼠学习记忆能力的变化,探讨其发生机制.方法 健康SD大鼠48只,按染氟剂量分为对照、低氟、高氟3组.低氟组、高氟组大鼠以燃煤型地方病氟中毒重病区燃煤烘烤的当地玉米为主要饲料,复制氟中毒大鼠模型,实验期为3、6个月,各8只大鼠.实验结束时用Morris水迷宫方法检测大鼠行为学变化,并用比色法测定脑组织乙酰胆碱酯酶和丁酰胆碱酯酶活性.结果 染氟剂量对逃避潜伏期时间、第7天穿过平台次数、逗留平台象限时间有明显影响(F值分别为29.29、6.47、6.50,P均<0.01):染氟时间对第7天穿过平台次数和逗留平台象限时间有明显影响(F值分别为16.11、45.59,P均<0.01);染氟剂量和时间对第7天穿过平台次数和逗留平台象限时间有交互作用(F值分别为4.67、5.68,P<0.05或<0.01).3个月时,高氟组大鼠逃避潜伏期时间[(14.71±4.85)s]较对照组[(9.28±4.22)s]明显增加(P<0.05);6个月时,低氟组、高氟组大鼠逃避潜伏期时间[(12.42±8.03)、(17.48±8.05)s]较对照组[(7.04±3.29)s]延长(P均<0.05),高氟组第7天穿过平台次数[(1.62±0.87)次]和逗留平台象限时间[(16.70±5.02)s]较对照组[(3.53±1.67)次、(23.33±5.35)s]降低(P均<0.05).染氟剂量对乙酰胆碱酯酶与丁酰胆碱酯酶活性均有明显影响(F值分别为12.83、13.27,P均<0.01);染氟时间对丁酰胆碱酯酶活性有明显影响(F=16.26,P<0.01).3个月时,低氟组丁酰胆碱酯酶活性[(0.55±0.12)kU/g]明显低于对照组[(0.73±0.10)kU/g,P<0.05],高氟组乙酰胆碱酯酶[(0.62±0.42)kU/g]和丁酰胆碱酯酶活性[(0.58±0.10)kU/g]均明显低于对照组[(1.41±0.52)、(0.73±0.10)kU/g,P均<0.05].胆碱酯酶活性与逃避潜伏期时间呈负相关(r=-0.68,P<0.01),胆碱酯酶活性与逗留平台象限时间呈正相关(r=0.57,P<0.01).结论 燃煤污染型慢性氟中毒大鼠学习记忆能力减退,可能与脑组织胆碱酯酶活性下降有关,二者间有量效关系.     

骨桥蛋白在不同营养条件下氟中毒大鼠肝组织中的表达及意义

目的探讨骨桥蛋白（OPN）在氟中毒大鼠肝组织中的表达及其意义。方法通过给予48只Wistar大鼠不同钙营养状况、不同蛋白营养状况和投氟剂量的固体饲料,复制氟中毒大鼠模型,6个月后提取各组大鼠肝组织,应用免疫组化技术及RT-PCR技术检测OPN的表达水平。结果大鼠肝脏OPNmRNA表达及蛋白平均表达水随着大鼠骨氟含量的增加而依次增强。结论氟可促进大鼠肝组织OPN表达,并且过量氟和低钙、低蛋白对促进大鼠肝组织OPN表达具有协同作用,而且OPN的表达与氟中毒机体损伤的程度密切相关。     

小剂量阿托品治疗重度有机磷农药中毒的临床研究

目的：评价小剂量阿托品治疗重度有机磷农药中毒的临床疗效。方法：观察组46例重度有机磷农药中毒患者,采用小剂量阿托品方案治疗;与采用传统方法治疗的对照组42例进行比较。结果：①观察组46例全部治愈,阿托品总用量最小5mg,最大46mg,平均（10.26±2.28）mg。对照组死亡5例,死亡率为11.9%。观察组治愈率显著高于对照组（P〈0.05）。②观察组无一例发生阿托品中毒、反跳和中间综合征（IMS）,对照组阿托品中毒18例（42.9%）、反跳4例（9.52%）、IMS4例（9.52%）,组间差异有统计学意义（P〈0.05）。结论：小剂量阿托品治疗重度有机磷农药中毒治愈率高,严重并发症发生率低。     

口服有机磷农药中毒合并上消化道出血58例临床分析

目的：探讨口服有机磷农药中毒合并上消化道出血的原因及治疗。方法：回顾分析本院58例急性有机磷农药口服中毒合并上消化道出血的原因及治疗效果。结果：58例患者中,治愈51例（87.9%）,死亡7例（12.1%）,出血原因主要为急性胃黏膜病变和应激性溃疡。结论：有机磷农药中毒合并上消化道出血,早发现、早预防、早治疗,效果良好。     

盐酸戊乙奎醚联合阿托品治疗有机磷农药中毒的应用

目的观察盐酸戊乙奎醚联合阿托品治疗急性有机磷农药中毒的临床疗效。方法 102例急性有机磷农药中毒的患者随机分为盐酸戊乙奎醚＋阿托品组和阿托品治疗组,两组同时给予氯解磷定治疗。结果盐酸戊乙奎醚＋阿托品组与阿托品治疗组比较,在中毒症状消失时间、阿托品化时间、恢复时间、血胆碱脂酶恢复时间、平均住院天数上均有显著性差异。盐酸戊乙奎醚＋阿托品组不良反应较阿托品治疗组明显减少。结论盐酸戊乙奎醚联合阿托品救治急性有机磷农药中毒副作用少、疗效高、安全可靠。     

可乐定急性中毒80例院外急救和急诊科教治效果分析

目的总结急性集体药物中毒事件院外急救和急诊科救治及组织经验,以进一步提高急性集体药物中毒事件的救治效果。方法回顾性总结北京市怀柔区某餐厅“4．23”可乐定中毒事件80例患者院外急救和急诊科内救治及组织的相关资料。结果经院外及时救治,院外与院内高效绿色通道开通,急诊科正确救治,本组80例中毒患者,留观35例,转往三级甲等医院45例,经治疗全部康复。结论对于急性集体药物中毒事件,全区应急系统密切配合协调,院内院外应急绿色通道畅通高效,可以提高抢救成功率。     

参麦注射液对百草枯所致肺损伤的保护作用

目的探讨参麦注射液在百草枯中毒所致肺损伤中的作用。方法120只SD大鼠随机分为百草枯中毒组（APP）,参麦注射液治疗组（SM1,SM2,SM3）。HE染色观察参麦注射液治疗组组织结构变化,采用免疫组织化学法测定各组肺组织中TGF—β1、IL-1β的表达水平。结果百草枯中毒组肺组织充血水肿明显,肺泡破坏严重,治疗组有所减轻;各治疗组与百草枯中毒组之间转化生长因子β-1（TGF—β1）,白细胞介素-1β（IL—1β）水平均较治疗组明显降低,各治疗组随剂量的增加,TGF-β1,IL-1β水平有明显下降,差异有显著性（P〈0．05）。结论参麦注射液在百草枯所致中毒大鼠肺损伤中能使TGF—β1,IL-1β表达水平下调,减轻肺泡炎症和充血程度,减轻百草枯中毒所致肺损伤,延缓和抑制肺纤维化的发生、发展。     

Improving Impact Poly(propylene) Morphology and Production: Selective Poisoning of Catalyst Surface Sites and the Use of Antistatic Agents

Summary: Selective poisoning has been studied as a means of improving the morphology and rheological properties of high‐impact poly(propylene) copolymer particles. Two different methods of poisoning the catalyst surface in order to avoid the accumulation of ethylene‐propylene rubber (EPR) without influencing the reaction kinetics were tested: a slurry‐phase poisoning step using ethylene glycol dimethyl ether between the homopolymerisation and copolymerisation reaction steps; and direct poisoning via the use of a commercial antistatic agent during the gas‐phase copolymerisation reactor. It was observed that both methods eliminated the formation of rubber on the particle surface without noticeably influencing the kinetics. On the other hand, the use of the products directly in the gas‐phase reaction also contributed to the reduction of static electricity. It can be concluded from these experiments that industrial antistatic agents derive at least part of their effect from poisoning of the active sites on the surface of the catalyst. Furthermore, it appears that in the case of the catalyst used in this study, EPR does not appear to flow out of the growing particles. Most of the EPR found at the surface of the particles is formed close to it.

SEM images of hiPP and GLYM001.     

Anticholinergic syndrome due to 'Devil's herb': when risks come from the ancient time

We describe a case of Mandragora autumnalis poisoning which occurred in a 72-year-old female patient who had eaten the venenous M. Autumnalis, picked near her home, mistaking it for the edible Borago Officinalis. M. Autumnalis is a solanaceous plant, common in the Sicilian countryside, which contains a variable concentration of solanum alkaloids, causing gastrointestinal irritation, and tropane alkaloids, with anticholinergic properties. Unluckily, M. Autumnalis is often mistaken for the edible B. Officinalis, likewise widespread in Sicilian countryside. The diagnosis of Mandragora poisoning was made on the basis of clinical symptoms and signs of anticholinergic syndrome associated with a history of vegetable meal of uncontrolled origin, moreover analysing the vegetable obtained from gastric lavage. Decontamination and symptomatic treatment were useful in our patient to control acute poisoning.     

Treatment of poisoning induced cardiac impairment using cardiopulmonary bypass: a review

Severe poisoning can cause potentially fatal cardiac depression. Cardiopulmonary bypass (CPB) can support the depressed myocardium, but there are no clear indications or guidelines available on its use in severe poisoning. A review was conducted of relevant papers in the available literature (seven single case reports of both deliberate and accidental ingestion of cardiotoxic drugs and two animal studies). Although CPB is rarely used in the management of poisoning, it may have potential benefits for haemodynamic instability not responding to conventional measures. At present there is insufficient evidence concerning the use of CPB as a treatment for severe cardiac impairment due to poisoning (grade C). This review suggests that in patients with severe and potentially prolonged reversible cardiotoxicity there is potential for full survival with CPB, provided that the patient has not already sustained hypoxic cerebral damage due to resistant hypotension prior to its use.