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作 者:邢英琦[1] 江新梅[1] 杨薇[1] 孙宏侠[2]
机构地区:[1]吉林大学第一医院神经内科,吉林长春130021 [2]吉林省人民医院神经内科,吉林长春130021
出 处:《中风与神经疾病杂志》2005年第3期251-253,i002,共4页Journal of Apoplexy and Nervous Diseases
摘 要:目的了解甲胺磷中毒迟发性神经病的肌肉病理变化特点,探讨地塞米松对有机磷中毒迟发性神经病(OPIDN)的保护作用。方法Leghorn产卵母鸡随机分为3组,A组:不染毒;B组:染毒+地塞米松治疗;C组:染毒+盐水。甲胺磷经消化道染毒,从染毒后第2天开始B、C组分别每天给地塞米松和生理盐水1周。染毒后1、2、3、4、8周末取鸡小腿腓肠肌制成光镜和电镜样品。结果病变主要表现为散在分布的节段性肌纤维坏死,坏死区及肌间质大量吞噬细胞浸润。B组腓肠肌坏死面积百分比在第3、4、8周与C组相比有显著性差异(P<0.05),第3周型纤维和型纤维等效直径与C组比较也有显著性差异。结论地塞米松对OPIDN肌肉病变有保护作用,但不能防止OPIDN的发生。Objective To study the characteristics of the muscular pathological changes on delayed neuropathy induced by methamidophos and inqured the protective effects of dexamethasone to the organophosphate induced delayed neuropathy(OPIDN). Methods 55 White Leghorn chicken were randomly divided into three groups:group A,the normal control group;group B,methemidophos poisoning with dexamethasone treatment;group C,methamidophos poisoning with saline injection. Since the second day of the orally methemidophos poisoning,dexamethasone was given to group B and saline to group C daily for one week. At the end of 1,2,3,4,8 week after poisoning,muscular samples of gastrocnemius were taken from the hens’calf and were observed with optical and electronic microscope. Results It showed that necrosis of segments of muscle fibers and macrophages infiltration were scattering distribution in observations of the necrosis area and muscular interstition. At the end of 3,4,8 week,there were significant differences in the area of muscular necrosis between group B and C. At the end of the third week,significant differences were also found in the equivalent diameter of type Ⅰ and Ⅱfiber. Conclusion It is suggested that the dexamethasone may have protective effects on muscular changer of OPIDN. However,it may not prevent OPIDN from developing.
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