中华劳动卫生职业病杂志
中華勞動衛生職業病雜誌
중화노동위생직업병잡지
CHINESE JOURNAL OF INDUSTRIAL HYGIENE AND OCCUPATIONAL DISEASES
2014年
4期
289-292
,共4页
王霞%高恒波%姚冬奇%田英平%苏建玲%张宏顺%孙承业%石汉文
王霞%高恆波%姚鼕奇%田英平%囌建玲%張宏順%孫承業%石漢文
왕하%고항파%요동기%전영평%소건령%장굉순%손승업%석한문
中毒,毒鼠强%乙酰胺%病理,脑皮层
中毒,毒鼠彊%乙酰胺%病理,腦皮層
중독,독서강%을선알%병리,뇌피층
Poisoning%Tetramine%Acetamide%Pathology%Cerebral cortex
目的 观察不同剂量乙酰胺对毒鼠强(tetramine,TET)中毒大鼠脑皮层组织病理学改变,为应用乙酰胺治疗TET中毒提供依据.方法 二级SD大鼠80只,随机分为生理盐水对照组、二甲基亚砜水溶液对照组、TET染毒组、2.88 g/kg·d-1乙酰胺治疗组和5.68 g/kg·d-1乙酰胺治疗组,每组16只动物.染毒组和治疗组禁食后给予TET灌胃染毒,染毒后分别肌注生理盐水和不同剂量乙酰胺,连续5d,并分别于治疗处理后3h、12h、48 h和7d取材,取材后通过光学显微镜和电子显微镜观察脑皮层组织病理学改变.结果 (1)光学显微镜观察:TET染毒组主要为脑皮层组织缺氧性改变,随时间延长逐渐加重,给予乙酰胺治疗后缺氧性改变有所减轻,2.88 g/kg·d-1乙酰胺治疗组较5.68 g/kg·d-1乙酰胺治疗组减轻明显.(2)电子显微镜观察:TET染毒后的主要改变为神经元细胞呈凋亡样改变;给予乙酰胺治疗后凋亡样改变的细胞不同程度减少,2.8 g/kg·d-1乙酰胺治疗组较5.6 g/kg·d1乙酰胺治疗组减少明显.结论 给予乙酰胺治疗后,未发现与TET协同作用的中枢毒性作用的脑皮层病理学表现,且给予2.8 g/kg·d-1乙酰胺治疗可能在一定程度减轻中毒后中枢神经损害,而增加乙酰胺治疗剂量,其改善中枢损害的作用有限.
目的 觀察不同劑量乙酰胺對毒鼠彊(tetramine,TET)中毒大鼠腦皮層組織病理學改變,為應用乙酰胺治療TET中毒提供依據.方法 二級SD大鼠80隻,隨機分為生理鹽水對照組、二甲基亞砜水溶液對照組、TET染毒組、2.88 g/kg·d-1乙酰胺治療組和5.68 g/kg·d-1乙酰胺治療組,每組16隻動物.染毒組和治療組禁食後給予TET灌胃染毒,染毒後分彆肌註生理鹽水和不同劑量乙酰胺,連續5d,併分彆于治療處理後3h、12h、48 h和7d取材,取材後通過光學顯微鏡和電子顯微鏡觀察腦皮層組織病理學改變.結果 (1)光學顯微鏡觀察:TET染毒組主要為腦皮層組織缺氧性改變,隨時間延長逐漸加重,給予乙酰胺治療後缺氧性改變有所減輕,2.88 g/kg·d-1乙酰胺治療組較5.68 g/kg·d-1乙酰胺治療組減輕明顯.(2)電子顯微鏡觀察:TET染毒後的主要改變為神經元細胞呈凋亡樣改變;給予乙酰胺治療後凋亡樣改變的細胞不同程度減少,2.8 g/kg·d-1乙酰胺治療組較5.6 g/kg·d1乙酰胺治療組減少明顯.結論 給予乙酰胺治療後,未髮現與TET協同作用的中樞毒性作用的腦皮層病理學錶現,且給予2.8 g/kg·d-1乙酰胺治療可能在一定程度減輕中毒後中樞神經損害,而增加乙酰胺治療劑量,其改善中樞損害的作用有限.
목적 관찰불동제량을선알대독서강(tetramine,TET)중독대서뇌피층조직병이학개변,위응용을선알치료TET중독제공의거.방법 이급SD대서80지,수궤분위생리염수대조조、이갑기아풍수용액대조조、TET염독조、2.88 g/kg·d-1을선알치료조화5.68 g/kg·d-1을선알치료조,매조16지동물.염독조화치료조금식후급여TET관위염독,염독후분별기주생리염수화불동제량을선알,련속5d,병분별우치료처리후3h、12h、48 h화7d취재,취재후통과광학현미경화전자현미경관찰뇌피층조직병이학개변.결과 (1)광학현미경관찰:TET염독조주요위뇌피층조직결양성개변,수시간연장축점가중,급여을선알치료후결양성개변유소감경,2.88 g/kg·d-1을선알치료조교5.68 g/kg·d-1을선알치료조감경명현.(2)전자현미경관찰:TET염독후적주요개변위신경원세포정조망양개변;급여을선알치료후조망양개변적세포불동정도감소,2.8 g/kg·d-1을선알치료조교5.6 g/kg·d1을선알치료조감소명현.결론 급여을선알치료후,미발현여TET협동작용적중추독성작용적뇌피층병이학표현,차급여2.8 g/kg·d-1을선알치료가능재일정정도감경중독후중추신경손해,이증가을선알치료제량,기개선중추손해적작용유한.
Objective To observe the effect of different doses of acetamide on the histopathology in the cerebral cortex of rats with tetramine (TET) poisoning and to provide a basis for the treatment of fluoroacetamide poisoning with acetamide.Methods Eighty clean Sprague-Dawley rats were randomly divided into five groups:saline control group,dimethyl sulfoxide water solution control group,TET poisoning group,acetamide (2.88 g/kg/d)treatment group,and acetamide (5.68 g/kg/d) treatment group,with 16 rats in each group.Rats in the poisoning group and treatment groups were poisoned with TET by intragastric administration after fasting; then,saline was injected intramuscularly into rats of the poisoning group,and different doses of acetamide were injected intramuscularly into rats of treatment groups; the course of treatment was 5 d.At 3 h,12 h,48 h,and 7 d after treatment,the cerebral cortex was harvested from rats in each group,and the histopathological changes in the cerebral cortex were evaluated under light and electron microscopes.Results The light microscopy showed that the TET poisoning group had hypoxia changes in the cerebral cortex,which worsened over time; the treatment groups had reduced hypoxia changes,and the acetamide (2.88 g/kg/d) treatment group had more reduction than the acetamide (5.68 g/kg/d) treatment group.The electron microscopy showed that the apoptosis of neuronal cells were the main pathological changes in the TET poisoning group; the treatment groups had reduced apoptotic changes,and the acetamide (2.88 g/kg/d) treatment group had more reduction than the acetamide (5.68 g/kg/d) treatment group.Conclusion No pathological changes associated with the synergistic toxic effect of acetamide and TET are found in the cerebral cortex.Acetamide (2.88 g/kg/d) could reduce central nervous lesions,but the efficacy is not improved after increasing the dose.For patients who cannot be identified with TET or fluoroacetamide poisoning,acetamide could be considered for treatment.