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作 者:邱泽武[1] 赵德禄[2] 史寅奎[1] 黄韶清[1] 刘艳琴[2]
机构地区:[1]军事医学科学院附属医院急诊科,北京100039 [2]军事医学科学院毒物药物研究所
出 处:《中国急救医学》2001年第2期71-72,共2页Chinese Journal of Critical Care Medicine
摘 要:目的 探讨氧化乐果中毒致呼吸肌麻痹的形成过程 ,寻找防治呼吸肌麻痹的合理方案。方法 所有实验大鼠均给予同等程度 ( 2LD50 )染毒 ,采用MS - 30 2生理药理分析仪测定经阿托品或阿托品加氯磷定治疗组与空白对照组大鼠的游离膈神经 -膈肌的收缩功能。结果 阿托品治疗组大鼠与空白对照组大鼠的单收缩和强直收缩有明显区别 (P <0 0 1) ,而阿托品加氯磷定治疗组大鼠与空白对照组大鼠的单收缩和强直收缩无明显的区别 (P >0 0 5 )。结论 早期合理应用阿托品和氯磷定治疗 ,能有效地对抗呼吸中枢抑制 ,并防止外周呼吸肌麻痹的发生。Objective The study was designed to examine the mechanism of respiratory muscle paralysis by acute omethomate poisoning. Methods Rats were administered in vivo with same doses of omethomate(2LD 50 ) and rats were treated with atropine or atropine plus PAM-CI. The function of isolated rats phrenic diaphragm was observed by MS-302 analyses instrument in physiology and pharmacology. Results In atropine group the function of isolated rats phrenic diaphragm was significantly less than that in control group ( P< 0.01). In atropine plus PAM-CI group the function of isolated rats phrenic diaphragm was similar to control group. Conclusion The reason of respiratory muscle paralysis may be related to the unreasonable treatment between atropine and PAM-CI. [
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