中国危重病急救医学
中國危重病急救醫學
중국위중병급구의학
CHINESE CRITICAL CARE MEDICINE
2010年
4期
197-200,前插1
,共5页
胆碱酯酶抑制剂%宾赛克嗪%二胺氧化酶%D-乳酸%肠屏障功能
膽堿酯酶抑製劑%賓賽剋嗪%二胺氧化酶%D-乳痠%腸屏障功能
담감지매억제제%빈새극진%이알양화매%D-유산%장병장공능
Cholinesterase inhibitor agents%Benthiactzine%Diamine oxidase%D-lactate%Gut barrier function
目的 观察胆碱酯酶抑制剂类神经性毒剂中毒后大鼠肠屏障功能和组织形态结构的变化以及宾赛克嚷的治疗作用.方法 40只雄性Wistar大鼠按随机数字表法均分为对照组、维埃克斯染毒模型组及宾赛克嗪1、3、9 mg/kg治疗组.皮下注射维埃克斯13μg/kg染毒;宾赛克嗪组在染毒后5 min腹腔注射相应剂量药物.各组于染毒后3 h取血,检测血浆D-乳酸浓度及二胺氧化酶(DAO)活性;同时取小肠组织,观察肠黏膜形态和超微结构变化.结果 与对照组比较.模型组血浆D-乳酸浓度和DAO活性均明显升高[D-乳酸:(87.752±22.906)mg/L比(29.072±6.546)mg/L,DAO:(6.72±0.93)U/L比(2.99±0.43)U/L,均P<0.01];宾赛克嗪1、3、9 mg/kg组呈现剂量依赖性降低血浆D-乳酸浓度和DAO活性,其中宾赛克嗪9 mg/kg组可逆转染毒后血浆D-乳酸浓度[(45.290±11.141)mg/L]和DAO活性C(3.17±0.68)U/L]增高(均P<0.01).光镜下观察模型组大鼠空肠和回肠肠壁变薄,皱壁变短,结构紊乱,固有层毛细血管扩张充血,黏膜间质水肿等病理变化;电镜下观察模型组大鼠回肠上皮细胞发生坏死,细胞器损伤,紧密连接破坏等变化.宾赛克嗪1、3、9 mg/kg组呈现剂量依赖性抑制小肠的病理变化.结论 胆碱酯酶抑制剂中毒时出现肠黏膜上皮细胞损伤,肠黏膜屏障功能破坏,通透性增加;宾赛克嗪能抑制中毒肠黏膜屏障结构和功能的损伤.
目的 觀察膽堿酯酶抑製劑類神經性毒劑中毒後大鼠腸屏障功能和組織形態結構的變化以及賓賽剋嚷的治療作用.方法 40隻雄性Wistar大鼠按隨機數字錶法均分為對照組、維埃剋斯染毒模型組及賓賽剋嗪1、3、9 mg/kg治療組.皮下註射維埃剋斯13μg/kg染毒;賓賽剋嗪組在染毒後5 min腹腔註射相應劑量藥物.各組于染毒後3 h取血,檢測血漿D-乳痠濃度及二胺氧化酶(DAO)活性;同時取小腸組織,觀察腸黏膜形態和超微結構變化.結果 與對照組比較.模型組血漿D-乳痠濃度和DAO活性均明顯升高[D-乳痠:(87.752±22.906)mg/L比(29.072±6.546)mg/L,DAO:(6.72±0.93)U/L比(2.99±0.43)U/L,均P<0.01];賓賽剋嗪1、3、9 mg/kg組呈現劑量依賴性降低血漿D-乳痠濃度和DAO活性,其中賓賽剋嗪9 mg/kg組可逆轉染毒後血漿D-乳痠濃度[(45.290±11.141)mg/L]和DAO活性C(3.17±0.68)U/L]增高(均P<0.01).光鏡下觀察模型組大鼠空腸和迴腸腸壁變薄,皺壁變短,結構紊亂,固有層毛細血管擴張充血,黏膜間質水腫等病理變化;電鏡下觀察模型組大鼠迴腸上皮細胞髮生壞死,細胞器損傷,緊密連接破壞等變化.賓賽剋嗪1、3、9 mg/kg組呈現劑量依賴性抑製小腸的病理變化.結論 膽堿酯酶抑製劑中毒時齣現腸黏膜上皮細胞損傷,腸黏膜屏障功能破壞,通透性增加;賓賽剋嗪能抑製中毒腸黏膜屏障結構和功能的損傷.
목적 관찰담감지매억제제류신경성독제중독후대서장병장공능화조직형태결구적변화이급빈새극양적치료작용.방법 40지웅성Wistar대서안수궤수자표법균분위대조조、유애극사염독모형조급빈새극진1、3、9 mg/kg치료조.피하주사유애극사13μg/kg염독;빈새극진조재염독후5 min복강주사상응제량약물.각조우염독후3 h취혈,검측혈장D-유산농도급이알양화매(DAO)활성;동시취소장조직,관찰장점막형태화초미결구변화.결과 여대조조비교.모형조혈장D-유산농도화DAO활성균명현승고[D-유산:(87.752±22.906)mg/L비(29.072±6.546)mg/L,DAO:(6.72±0.93)U/L비(2.99±0.43)U/L,균P<0.01];빈새극진1、3、9 mg/kg조정현제량의뢰성강저혈장D-유산농도화DAO활성,기중빈새극진9 mg/kg조가역전염독후혈장D-유산농도[(45.290±11.141)mg/L]화DAO활성C(3.17±0.68)U/L]증고(균P<0.01).광경하관찰모형조대서공장화회장장벽변박,추벽변단,결구문란,고유층모세혈관확장충혈,점막간질수종등병리변화;전경하관찰모형조대서회장상피세포발생배사,세포기손상,긴밀련접파배등변화.빈새극진1、3、9 mg/kg조정현제량의뢰성억제소장적병리변화.결론 담감지매억제제중독시출현장점막상피세포손상,장점막병장공능파배,통투성증가;빈새극진능억제중독장점막병장결구화공능적손상.
Objective To investigate the functional and morphological structure changes in the gut barrier of rats induced by cholinesterase inhibitor VX poisoning, and the therapeutic effect of benthiactzine. Methods Forty male Wistar rats were randomly divided into five groups: normal saline control group, VX poisoning (model) group, benthiactzine 1, 3, 9 mg/kg treatment groups, with 8 rats in each group. In the benthiactzine treatment groups, different dosages of the drug were respectively given (intraperitoneal injection) 5 minutes after VX poisoning (13 μg/kg subcutaneous injection). The plasma concentration of D-lactate and the diamine oxidase (DAO) activity, which reflected the gut barrier function, were measured at 3 hours after VX poisoning. At the same time point, the specimens from jejunum and ileum were harvested. The morphological changes in the intestinal mucosa were determined with light microscope and electron microscope. Results After VX poisoning, the plasma D-lactate concentration and the DAO activity in model group were significantly increased compared with those of control group [D-lactate concentration in model group was (87.752±22.906) mg/L which was higher than that of control group (29.072±6.546) mg/L; DAO activity in model group was (6.72±0.93) U/L which was higher than that of control group (2.99±0.43) U/L, both P<0.01]. These values could be decreased dose-dependently after benthiactzine 1, 3, 9 mg/kg administration after the VX poisoning. Furthermore, the increase in D-lactate (45.290±11.141) mg/L and DAO activity (3.17±0.68) U/L could be totally reversed by 9 mg/kg of benthiactzine (both P<0.01). In model group, the intestinal mucosal epithelial injury was obvious at 3 hours after VX poisoning as shown under light microscope, including diminution of the mucosal thickness and the height of villi in jejunum and ileum, interstitial edema, angiotelectasis. Also electronic microscopic examination revealed damaged organelles and cell tight junction of mucosal epithelium. These pathological changes in intestine could be inhibited by benthiactzine in dose-dependent manner. Conclusion The gut barrier function in rats was seriously damaged by the cholinesterase inhibitor agents poisoning, as a result of injury to intestinal mucosa and increase of intestinal permeability. Benthiactzine exerts protection against functional and morphological structure damages of the gut barrier during intoxication.
