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991.
Abstract Six male patients with severe ethylene glycol poisoning were studied with respect to the origin of the metabolic acidosis. The plasma concentrations of ethylene glycol were 4–41 mmol/l and treatment included alkali, ethanol and hemodialysis. Plasma analysis by isotachophoresis and whole blood lactate determinations showed that glycolate (17.0–29.3 mmol/l), lactate (1.4–6.2 mmol/l) and β-hydroxybutyrate (≤1.8 mmol/l) were present in elevated concentrations contributing to the acidosis. Oxalate (≤0.33 mmol/l), glyoxylate (<0.2 mmol/l) and formate (<0.4 mmol/l) concentrations were negligible and did not contribute to any significant degree to the acidosis. The elevated plasma glycolate concentration was highly correlated to the anion gap (r=0.923) and the glycolate made up for 96.1% (n=6, range 84.7–108.8) of the increased anion gap. We conclude that glycolate accumulation is the main reason for the metabolic acidosis in ethylene glycol poisoning. The mean dialysator (1.6 m2) clearances of glycolate at a blood flow of 200 ml/min in two patients were 137 ml/min (n=9, SD±8, range 125–149) and 144 ml/min (n=11, SD±8, range 133–158). By applying first order kinetics during hemodialysis a volume of distribution of glycolate of 0.55 l/kg was found, assuming that the dialysator clearance equals the total body clearance of glycolate. Thus glycolate, the probable main metabolite of ethylene glycol, is efficiently removed by hemodialysis.  相似文献   
992.
本文就高氟区小儿骨盆及正常小儿骨盆各75例作了X线对照观察,发现病区小儿骨盆的骨纹粗糙呈粗布状,排列不规则,并有颗粒状骨纹及骨斑。在股骨上端先期钙化带的下方出现硬化带,硬化带下部不规则。上述改变是诊断小儿氟骨症的可靠依据。  相似文献   
993.
Summary The effect of phenobarbital and phenylbutazone treatment on the renal damage induced by the toxic mushroomCortinarius speciosissimus was studied in female rats. Phenobarbital sodium was given in drinking water (0.05% solution) for 11 days prior to the administration of mushroom. Phenylbutazone was given s.c. in doses of 50 and 100 mg/kg 1 h before the mushroom administration. Homogenized mushroom was given orally by stomach tube at a dose of 250 mg dried mushroom/kg body weight.It was found that the phenobarbital treatment strongly increased the damage induced byC. speciosissimus in the tubules of the kidney cortex but had no effect on the inflammation in the renal outer medullary zone induced by this toxic mushroom. Phenylbutazone treatment had no effect on the renal damage induced byC. speciosissimus.  相似文献   
994.
大鼠芥子气全身性中毒及地塞米松治疗   总被引:1,自引:0,他引:1  
芥子气LD_(70)中毒后,地塞米松0.35mg/kg腹腔注射,每日1次,中毒大鼠的活存率由29%提高到59%.死亡动物的活存时间也延长了23%,并使症状得到改善,腹泻及口、鼻分泌物明显减少,食量增加,一般状况较好.脏器检查发现,生理盐水对照组肾上腺重量增加57%,颜色变红;而治疗组只增加22%,色较正常.地塞米松合并庆大霉素及青霉素治疗,效果更好.实验结果首次证明适量的地塞米松对大鼠芥子气全身性中毒有一定的治疗作用,但过量反有害处.  相似文献   
995.
Dinophysistoxin-1, 35-methylokadaic acid, is a causative agent of diarrhetic shellfish poisoning. The biological activities and tumor-promoting activity of dinophysistoxin-1 were studied together with those of okadaic acid and 7-O-palmitoyl okadaic acid. Dinophysistoxin-1 is a skin irritant and induces ornithine decarboxylase in mouse skin with the same potency as okadaic acid. 7-O-Palmitoyl okadaic acid induced a lower activity than the other compounds. Dinophysistoxin-1 inhibited the specific [3H]okadaic acid binding to a participate fraction of mouse epidermis. The binding affinities of dinophysistoxin-1 and okadaic acid to a particulate fraction were almost the same. Dinophysistoxin-1 showed a tumor-promoting activity as strong as that of okadaic acid in a two-stage carcinogenesis experiment on mouse skin. The percentages of tumor-bearing mice in the groups treated with 100 μg of 7,12-dimethylbenz[α]anthracene (DMBA) followed by 5 μg of dinophysistoxin-1, twice a week, and with DMBA followed by 5 μg of okadaic acid twice a week were 86.7% and 80.0% in week 30, respectively. The average number of tumors per mouse was 4.6 in the former group and 3.9 in the latter. Dinophysistoxin-1 and okadaic acid act on cells through different pathways from the 12-O-tetradecanoylphorbol-13-acetate-type tumor promoters.  相似文献   
996.
Combined administration of 0.1% nitrite and 0.1% aminopyrine in the drinking water for eight to ten weeks resulted in subsequent development of both hepatocellular nodules and cholangiofibrotic lesions/cholangiocellular carcinomas in Syrian golden hamsters. Additional prior dosing with Opisthorchis viverrini metacercariae (100/animal) induced inflammatory and proliferative changes in the livers of infected hamsters and was associated with a significant increase in yields of hepatocellular and cholangiocellular preneoplastic and neoplastic lesions. Thus, environmental factors thought to be casually related to the high levels of human liver cancer observed in the Northeastern provinces of Thailand were sufficient to bring about development of equivalent tumors in experimental animals. The results indicate that parasite associated liver injury and non-specific compensatory regeneration may play an important role in generation of both hepatocellular and cholangiocellular carcinomas in man.  相似文献   
997.
目的:为了阐明我院损伤与中毒的收治情况及外部原因构成规律,为疾病的防治提供依据。方法:收集我院近十年住院病人的病历资料,按ICD编码进行准确分类和统计分析。结果:损伤与中毒病人占各类疾病的10.68%;在外部原因中以机动车辆交通事帮为最高。结论:损伤与中毒是住院病人的主要疾病之一,加强交通管理,施工和机器操作安全,增强防范意识,是减少损伤与中毒的重要因素。  相似文献   
998.
目的:评价齐墩果醇酸(OA)对急性肝损伤的保肝作用.方法:小鼠sc OA 200 μmol·kg~(-1)三天,然后给予肝毒物.通过病理组织学观察及测定血清丙氨酸转氨酶和艾杜糖醇脱氢酶活性来估价肝损伤.结果:OA能明显减轻四氯化碳,溴苯,醋氨酚,速尿,硫代乙酰胺,鬼笔毒环肽,秋水仙硷,氯化镉,D—半乳糖胺和内毒素等所致小鼠急性坏死性肝损伤,降低这些肝毒物所引起的血清转氨酶和艾杜糖醇脱氢酶的升高,但对氯仿,二甲亚硝氨,鹅膏菌索和烯丙醇的毒性无作用.结论:OA能减轻多种化学物质(但并非全部)引起的肝损伤.其保肝机制可能是多方面的.  相似文献   
999.
本文通过实验研究和10年临床、现场动态观察,探讨了工业性氟病的早期表现和防治措施。结果表明,尿氟、尿羟、骨氟、骨骼X线征象及病理改变与氟暴露呈剂量-反应关系;氟对骨外系统影响的早期表现为肾超微结构、肾酶和尿酶活性、免疫功能改变。通过动态观察,实施的车间改造、工艺改革、个人防护等,以及硼的预防性治疗等综合性防治措施已取得明显效果。  相似文献   
1000.
铅作业女工脑血流图分析王霞玲,于文华,王铁柱,王全治,孙丽珍,王燕华(内蒙古乌拉特前旗卫生防疫站,014400)对109名接铅女工进行脑血流图检查,主要以本地印刷、铸字、排字女工109名为调查对象,已婚102名,占93.5%,平均年龄32岁(24~4...  相似文献   
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