Objective To investigate the therapeutic effect and its mechanisms of benthiaczine on cholinesterase inhibitor VX poisoning by observing on the changes in plasma endotoxin content in mice.Methods Three hundred and six male Kunming mice were randomly assigned to five groups : normal group,VX poisoning (model) group, benthiaezine, atropine or 654-2 pretreatment group. The above mentioned drugs were respectively given 10 minutes before hypodermic injection of VX in a dose of 0.02 mg/kg. The plasma concentration of endotoxin was measured at 1.5, 3, 6, 24, 48 and 72 hours after VX poisoning.Results After VX injection, the endotoxin concentration in model group was significantly increased compared with normal group (all P<0.01). The endotoxin concentration in model group was (5.36±1.62) kEU/L at 1.5 hours, which was almost twice of that of normal group [(1.90±0.41) kEU/L]. It increased gradually to (11.47±3.90) kEU/L at 24 hours, which was 5 fold of that of the normal group (all P<0.01), and it maintained on the abnormally high level until 48 hours, then declined to the level of normal group after 72 hours. The endotoxin concentration of benthiaezine pretreatment group was significantly lower than that of model group at 1.5 hours and 3 hours after VX injection [(3.73±0.71) kEU/L, (3.95±1.26) kEU/L, respectively, P<0.01 and P<0.05], but there was no significant difference between two groups at 6 hours [(8.77±1.85) kEU/L] and 24 hours [(11.47±2.51) kEU/L],though it was significantly higher than normal group (both P<0.01). It lowered to the normal level at 48 hours. The endotoxin concentration in atropine pretreatment group was significantly higher than model group at 1.5-24 hours after VX injection (P<0.05 or P<0.01), while that of 654-2 pretreatment group reached a peak at 6 hours, which was significantly higher than that of the model group (P<0.01).Conclusion The increased endotoxin concentration induced by VX in mice 1.5-48 hours after poisoning can be reversed by pretreatment of benthiaczine, but aggravated by pretreatment of atropine or 654-2. The administration of benthiaczine could alleviate the injury to the gut barrier function thus delay translocation of endotoxin into blood, and also shorten the time of endotoxemia.%目的 观察新型抗毒剂宾赛克嗪对维埃克斯染毒后不同时间点小鼠血浆内毒素浓度变化的影响及其机制.方法 306只雄性昆明小鼠被随机分为正常对照组、维埃克斯染毒模型组以及宾赛克嗪、阿托品和山莨菪碱3个治疗组;各治疗组分别于皮下注射维埃克斯0.02 mg/kg染毒前10 min经腹腔注射相应药物.各组均于染毒后1.5、3、6、24、48和72 h取血,检测血浆内毒素浓度.结果 与正常对照组[内毒素浓度为(1.90±0.41)kEU/L]比较,模型组1.5 h血浆内毒素浓度为(5.36±1.62)kEU/L,升高了约2倍;之后逐渐升高,至24 h达高峰,浓度为(11.47±3.90)kEU/L,较正常对照组升高了约5倍(P均<0.01),异常增高可持续至48 h,72 h后恢复至正常对照组水平.宾赛克嗪治疗组在1.5 h和3 h时内毒素浓度分别为(3.73±0.71)kEU/L和(3.95±1.26)kEU/L,显著低于模型组(p<0.01和P<0.05);6 h和24 h血浆内毒素浓度分别为(8.77±1.85)kEU/L和(11.47±2.51)kEU/L,与模型组比较差异无统计学意义,但显著高于正常对照组(P均<0.01);至48 h恢复至正常对照组水平.在相同实验条件下,阿托品治疗组血浆内毒素浓度在1.5～24 h显著高于模型组(P<0.05或P<0.01);而山莨菪碱治疗组血浆内毒素浓度在6 h达高峰,显著高于模型组(P<0.01).结论 维埃克斯染毒后1.5～48 h小鼠血浆内毒素浓度显著增高,使用宾赛克嗪能减轻胃肠道黏膜屏障功能的损伤,延缓内毒素进入血中的速度,并能缩短内毒素在血中的停留时间.而使用阿托品和山莨菪碱后则能加重胃肠道黏膜屏障功能的损伤.
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