Qiu Zewu, Zhao Delu, Shi Yinkui, Huang Shaoqing
Department of Emergency, Beijing 307 Hospital, Beijing 100039, China.
Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2002 Oct;20(5):359-61.
To examine the therapeutic effect of combined use of obidoxime and atropine with artificial ventilation on respiratory muscle paralysis caused by omethoate poisoning in rats.
Rats were exposed to 2 times the dose of LD50 omethoate and treated with atropine (10 mg/kg) to counteract cholinergic symptoms. When the rats' respiratory frequency became slower and breathed with difficulty, the trachea intubation and artificial ventilation was carried out. The rats in group A were continuously treated with atropine. The dose of obidoxime for Group B, C and D were 8, 15, 20 mg/kg respectively, given at the same time as artificial ventilation and 1, 2, 3 hours later. The doses of atropine was reduced to 1/3 - 2/3 of the first dose so as to maintain the rats atropinized. If the rat survival was beyond 60 minutes after withdrawal of artificial ventilation, the combined treatment was considered successful. The function of isolated phrenic diaphragm of the rats was observed with MS-302 physiological and pharmacological analysis instrument.
None of the rats in Group A was successful after withdrawal from artificial ventilation and the function of phrenic diaphragm appeared poor; whereas > 80% of the rats in B, C, D Group were successful after withdrawal from artificial ventilation in 3 h and the function of phrenic diaphragm remained well. The survival rate in B, C and D groups were higher after withdrawal from artificial ventilation than that in Group A(P < 0.01). The function of phrenic diaphragm in Group B, C and D were gradually decreased after ACh was added into the container.
Combined use of suitable dose of obidoxime and atropine with artificial ventilation for respiratory muscle paralysis caused by omethoate poisoning could promote the recovery of diaphragm function and reduce the death rate in poisoned rats.
探讨氯解磷定与阿托品联用并结合人工通气对氧乐果中毒致大鼠呼吸肌麻痹的治疗效果。
大鼠经2倍LD50剂量的氧乐果染毒后,用阿托品(10mg/kg)对抗胆碱能症状。当大鼠呼吸频率减慢、呼吸困难时,行气管插管及人工通气。A组大鼠持续给予阿托品治疗。B、C、D组氯解磷定剂量分别为8、15、20mg/kg,在人工通气时及通气后1、2、3小时给予,阿托品剂量减至首剂量的1/3 - 2/3以维持大鼠阿托品化。若撤机后大鼠存活超过60分钟,则联合治疗视为成功。用MS - 302生理药理分析仪观察大鼠离体膈神经膈肌的功能。
A组大鼠撤机后均未成功,膈神经膈肌功能差;而B、C、D组>80%的大鼠在撤机3小时后成功,膈神经膈肌功能良好。B、C、D组撤机后的存活率高于A组(P<0.01)。向容器中加入乙酰胆碱后,B、C、D组膈神经膈肌功能逐渐下降。
合适剂量的氯解磷定与阿托品联用并结合人工通气治疗氧乐果中毒致呼吸肌麻痹,可促进膈肌功能恢复,降低中毒大鼠死亡率。