CAJ | 학술논문

目的评价宾赛克嗪对胆碱酯酶抑制剂敌敌畏中毒致呼吸衰竭(呼衰)的救治效果.方法将45只雄性Wistar大鼠按随机数字表法分为对照组、模型组及宾赛克嗪0.5、1.0、2.0 mg/kg救治组,每组9只.用敌敌畏腹腔注射累积染毒法制备大鼠有机磷农药中毒模型.观察染毒前、呼衰时及救治30 min内各组大鼠的症状、呼吸频率(RR)、动脉血气及电解质分析、血浆超氧化物歧化酶(SOD)和丙二醛(MDA)的变化以及肺组织病理改变.结果敌敌畏染毒至呼衰时,各组动物均出现不同程度的口唇及四肢发绀、惊厥.宾赛克嗪0.5、1.0和2.0 mg/kg组救治成功率分别为66.7%(6/9)、77.8%(7/9)和88.9%(8/9),存活动物于救治后1～5 min起症状逐渐缓解,30 min内全部恢复正常;RR也于救治后30 min恢复至染毒前水平.呼衰发生后,模型组动脉血氧分压(PaO_2)、动脉血氧饱和度(SaO_2)、SOD水平明显下降,MDA水平均明显升高,出现明显的呼吸性酸中毒合并代谢性酸中毒;宾赛克嗪各组救治后30 min,各指标均显著改善(P均<0.01),且均恢复至染毒前水平.光镜下模型组动物肺泡间隔增厚,肺泡壁和毛细血管壁充血、灶状出血,部分肺泡水肿及炎性细胞浸润;宾赛克嗪救治各组肺出血、淤血减轻,肺泡间隔肿胀减轻,未见肺泡内水肿.结论新型抗毒剂宾赛克嗪对有机磷农药引起的呼衰治疗效果良好.
목적 평개빈새극진대담감지매억제제활활외중독치호흡쇠갈(호쇠)적구치효과.방법 장45지웅성Wistar대서안수궤수자표법분위대조조、모형조급빈새극진0.5、1.0、2.0 mg/kg구치조,매조9지.용활활외복강주사루적염독법제비대서유궤린농약중독모형.관찰염독전、호쇠시급구치30 min내각조대서적증상、호흡빈솔(RR)、동맥혈기급전해질분석、혈장초양화물기화매(SOD)화병이철(MDA)적변화이급폐조직병리개변.결과 활활외염독지호쇠시,각조동물균출현불동정도적구진급사지발감、량궐.빈새극진0.5、1.0화2.0 mg/kg조구치성공솔분별위66.7%(6/9)、77.8%(7/9)화88.9%(8/9),존활동물우구치후1～5 min기증상축점완해,30 min내전부회복정상;RR야우구치후30 min회복지염독전수평.호쇠발생후,모형조동맥혈양분압(PaO_2)、동맥혈양포화도(SaO_2)、SOD수평명현하강,MDA수평균명현승고,출현명현적호흡성산중독합병대사성산중독;빈새극진각조구치후30 min,각지표균현저개선(P균<0.01),차균회복지염독전수평.광경하모형조동물폐포간격증후,폐포벽화모세혈관벽충혈、조상출혈,부분폐포수종급염성세포침윤;빈새극진구치각조폐출혈、어혈감경,폐포간격종창감경,미견폐포내수종.결론 신형항독제빈새극진대유궤린농약인기적호쇠치료효과량호.
Objective To investigate the therapeutic effects of benthiactzine against respiratory failure induced by cholinesterase inhibitor dimethyl dichloro-vinyl phosphate (DDVP) in rats. Methods Forty-five male Wistar rats were divided into five groups randomly: control group,model group,and benthiactzine 0.5,1.0,2.0 mg/kg treatment groups (each n=9). Rats were treated with DDVP by intraperitoneal injection to reproduce respiratory failure model. The symptoms,respiratory rate (RR),blood gas analysis,electrolyte and plasma superoxide dismutase (SOD),malondialdehyde (MDA) and the pathological changes were observed before poisoning,during respiratory failure,and in different periods after the treatment. Results In rats with respiratory failure induced by DDVP,cyanosis and convulsion occurred in all groups. The success rates in three benthiactzine groups were 66.7% (6/9),77.8% (7/9) and 88.9% (8/9). The rats of benthiactzine treatment groups recovered in 15 minutes after treatment and returned to normal state in 30 minutes. RR also returned to normal in 30 minutes. When respiratory failure occurred,arterial oxygen partial pressure (PaO_2),arterial oxygen saturation (SaO_2) and plasma SOD were decreased,plasma MDA was increased,and mixed acidosis was found. Thirty minutes after the treatment of benthiactzine,all above parameters in three groups returned to normal (all P<0.01). In respiratory failure rats,pathological examination of lung tissue revealed dilatation of pulmonary vessels with aggregation of erythrocytes,widening of alveolar space with presence of red blood cells in alveoli with heavy infiltration of inflammatory cells,and pulmonary edema and hemorrhage. The lungs of rats treated with benthiactzine showed less intense pathological changes. Conclusion The new medicine against poisoning benthiactzine can be a favourable drug against respiratory failure induced by orgnaophosphorus pesticides.