Dibenzepine and its Metabolites in Blood,Muscle, Liver,Vitreous Body and Urine from Fatal Poisoning

Abstract: This paper presents a separation technique followed by spectrophotometry for the quantitative determination of dibenzepine and its main metabolites in autopsy material. The method, which has a lower detection limit of 0.5 μg/g material, was used for blood, tissue and urine from 8 cases in which dibenzepine was considered to be the only or a contributory cause of death. In addition to unchanged dibenzepine, three N-demethylated metabolites were detected and identified in the material. According to the results the material could be divided into two groups. One group, six cases, with high concentrations of total dibenzepine (dibenzepine plus metabolites), blood 23–147 μg/g, liver 255–566 μg/g, in which death was caused by dibenzepine alone or in combination with alcohol, and another group, two cases, with ten times lower total dibenzepine concentrations in blood and tissue; in this group additional factors might have contributed to death.     

Chelation in Metal Intoxication. III. Lowering of Nickel Content in Poisoned Rat Organs

Abstract Six metal binding agents were screened in vivo for their ability to mobilise nickel from the brain, heart, kidney and liver of nickel poisoned rats. Out of these, 1,2 cyclohexylene dinitrilotetraacetic acid (CDTA) was most effective in removing the metal from the heart (78 %) followed by brain (76 %), kidney (65 %) and liver (57 %) whereas diethyl-dithiocarbamate (DDC) was more effective in the order of heart (85 %), liver (51 %), kidney (44 %) and brain (32 %). Under in vitro conditions, CDTA, diethylene triaminepenta-acetic acid (DTPA) and nitrilotriacetic acid (NTA) were found to be more effective in dialysing out nickel from the subcellular fractions of liver and kidney and the blood corpuscles of rats prctreated with nickel sulphate. In general, no correlation between the chemical structure or molecular weight of the chelators and their ability to remove nickel from the biological system was observed.     

The effect of prior treatment with 4-dimethylaminophenol (DMAP) on animals experimentally poisoned with hydrogen cyanide

Six dogs were given sufficient oral 4-dimethylaminophenol (DMAP) to produce a peak methaemoglobin level of 12–15%. Five out of the six dogs then survived an intravenous injection of approximately 2 LD₅₀'s of hydrogen cyanide given when the methaemoglobin had reached 8–10%. The sixth dog died after 44 min. When the same dose of hydrogen cyanide was given to dogs, not previously given DMAP, all three died within 11/2 min. It was concluded that prior treatment with oral DMAP provided a large measure of protection against cyanide poisoning. Comparison of cyanide levels in whole blood and plasma in the two groups of dogs lent support to the hypothesis that methaemoglobin complexed with cyanide in the erythrocytes causing the plasma cyanide to remain lower than it did in unprotected animals.     

影响洗胃效果的原因分析

对口服药物中毒的１８例患者，进行经口插管洗胃，并分别留取洗出液进行毒物检测，目测洗出液澄清无味时留取最终标本检测毒物含量。结果最终标本毒物残留量最少０．４％，最多７６．７％，说明操作者用目测洗胃液澄清度或闻及气味来判断洗胃是否彻底的方法是影响洗胃效果的重要因素。另外，对影响洗胃效果的其它因素（如药物的理化性质、洗胃液及患者的体位等）进行了分析。     

慢性铅性肾病的肾脏病理

对９例慢性铅性肾病患者进行了肾活检，并分别作免疫荧光、光镜和电镜检查。结果发现，肾小球和肾小管均有不同程度的损害。总结了铅性肾病肾脏病理特点，计数了肾小管上皮细胞异常线粒体的数目。     

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。     

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.