中国中西医结合急救杂志
中國中西醫結閤急救雜誌
중국중서의결합급구잡지
INTEGRATED TRADITIONAL CHINESE AND WESTERN MEDICINE IN PRACTICE OF CRITICAL CARE MEDICINE
2014年
1期
55-57
,共3页
何国鑫%汤旭明%郑霞%潘升华%翁海旭%罗文朝%李海林
何國鑫%湯旭明%鄭霞%潘升華%翁海旭%囉文朝%李海林
하국흠%탕욱명%정하%반승화%옹해욱%라문조%리해림
有机磷农药中毒,急性%膈肌%ATP酶%血必净注射液
有機燐農藥中毒,急性%膈肌%ATP酶%血必淨註射液
유궤린농약중독,급성%격기%ATP매%혈필정주사액
Acute organophosphorus poisoning%Diaphragm%ATPase%Xuebijing injection
目的:探讨急性有机磷农药中毒(AOPP)大鼠膈肌ATP酶活性变化及血必净的治疗作用。方法选择24只健康SD大鼠按随机原则分为对照组、模型组及血必净治疗组,每组8只;给大鼠灌胃氧化乐果50 mg/kg复制成AOPP模型;血必净治疗组腹腔注射血必净注射液10 mL/kg,对照组、模型组腹腔注射等量生理盐水。各组分别于制模后6 h采用酶联免疫吸附试验(ELISA)检测膈肌Na+-K+-ATP酶和Ca2+-ATP酶活性,光镜下观察各组大鼠膈肌组织病理形态学变化。结果模型组Na+-K+-ATP酶活性在染毒后6 h明显低于对照组(mmol?h-1?g-1:5.22±0.74比9.98±0.37,P<0.01);血必净治疗组Na+-K+-ATP酶活性在染毒后6 h(6.93±1.14)明显高于于模型组(P<0.05);模型组Ca2+-ATP酶活性在染毒后6 h明显低于对照组(mmol?h-1?g-1:7.45±0.74比12.08±0.74,P<0.01),血必净治疗组Ca2+-ATP酶活性(9.35±1.67)明显高于模型组(P<0.05)。光镜下观察:模型组出现膈肌肿胀,坏死,血必净治疗组未发现坏死。结论 AOPP大鼠膈肌可出现变性坏死,采用血必净干预可减轻膈肌组织损伤,其机制可能与降低膈肌Na+-K+-ATP酶和Ca2+-ATP酶活性有关。
目的:探討急性有機燐農藥中毒(AOPP)大鼠膈肌ATP酶活性變化及血必淨的治療作用。方法選擇24隻健康SD大鼠按隨機原則分為對照組、模型組及血必淨治療組,每組8隻;給大鼠灌胃氧化樂果50 mg/kg複製成AOPP模型;血必淨治療組腹腔註射血必淨註射液10 mL/kg,對照組、模型組腹腔註射等量生理鹽水。各組分彆于製模後6 h採用酶聯免疫吸附試驗(ELISA)檢測膈肌Na+-K+-ATP酶和Ca2+-ATP酶活性,光鏡下觀察各組大鼠膈肌組織病理形態學變化。結果模型組Na+-K+-ATP酶活性在染毒後6 h明顯低于對照組(mmol?h-1?g-1:5.22±0.74比9.98±0.37,P<0.01);血必淨治療組Na+-K+-ATP酶活性在染毒後6 h(6.93±1.14)明顯高于于模型組(P<0.05);模型組Ca2+-ATP酶活性在染毒後6 h明顯低于對照組(mmol?h-1?g-1:7.45±0.74比12.08±0.74,P<0.01),血必淨治療組Ca2+-ATP酶活性(9.35±1.67)明顯高于模型組(P<0.05)。光鏡下觀察:模型組齣現膈肌腫脹,壞死,血必淨治療組未髮現壞死。結論 AOPP大鼠膈肌可齣現變性壞死,採用血必淨榦預可減輕膈肌組織損傷,其機製可能與降低膈肌Na+-K+-ATP酶和Ca2+-ATP酶活性有關。
목적:탐토급성유궤린농약중독(AOPP)대서격기ATP매활성변화급혈필정적치료작용。방법선택24지건강SD대서안수궤원칙분위대조조、모형조급혈필정치료조,매조8지;급대서관위양화악과50 mg/kg복제성AOPP모형;혈필정치료조복강주사혈필정주사액10 mL/kg,대조조、모형조복강주사등량생리염수。각조분별우제모후6 h채용매련면역흡부시험(ELISA)검측격기Na+-K+-ATP매화Ca2+-ATP매활성,광경하관찰각조대서격기조직병리형태학변화。결과모형조Na+-K+-ATP매활성재염독후6 h명현저우대조조(mmol?h-1?g-1:5.22±0.74비9.98±0.37,P<0.01);혈필정치료조Na+-K+-ATP매활성재염독후6 h(6.93±1.14)명현고우우모형조(P<0.05);모형조Ca2+-ATP매활성재염독후6 h명현저우대조조(mmol?h-1?g-1:7.45±0.74비12.08±0.74,P<0.01),혈필정치료조Ca2+-ATP매활성(9.35±1.67)명현고우모형조(P<0.05)。광경하관찰:모형조출현격기종창,배사,혈필정치료조미발현배사。결론 AOPP대서격기가출현변성배사,채용혈필정간예가감경격기조직손상,기궤제가능여강저격기Na+-K+-ATP매화Ca2+-ATP매활성유관。
Objective To investigate the changes in ATPase activity of diaphragm in rats with acute organophosphorus poisoning (AOPP) and to explore the effect of Xuebijing injection on the ATPase activity. Methods 24 clean healthy Spraue-Dawley(SD)rats were divided into control group,model group and Xuebijing treatment group by means of random number table,with 8 rats in each group. AOPP model was established by intra-gastrical administration of 50 mg/kg oxide dimethoate. In Xuebijing treatment group,after oxide dimethoate administration,intraperitoneal injection of Xuebijing(10 mL/kg)was given at the same time,while in control group and model group,equal amount of normal saline(NS)was injected via the same route. The rats were sacrificed at 6 hours after model formation,and their diaphragms were taken sterilely. The activities of Na+-K+-ATPase and Ca2+-ATPsae of diaphragms were detected by enzyme linked immunosorbent assay(ELISA). The histopathological changes in diaphragms of rats were observed with light microscopy. Results 6 hours after intoxication,the diaphragm Na+-K+-ATPase activity of rats in model group was markedly lower than that in control group(mmol?h-1?g-1:5.22±0.74 vs. 9.98±0.37,P<0.01),while the Na+-K+-ATPase activity in Xuebijing treatment group(6.93±1.14) was markedly higher than that in model group(P<0.05). The diaphragm Ca2+-ATPase activity of rats in model group was markedly lower than that in control group(mmol?h-1?g-1:7.45±0.74 vs. 12.08±0.74,P<0.01),while the Ca2+-ATPase activity in Xuebijing treatment group(9.35±1.67)was obviously higher than that in model group(P<0.05)after intoxication for 6 hours. Light microscope observation indicated that there were swelling and necrosis in diaphragm in model group,while in Xuebijing treatment group no necrosis was found. Conclusion The diaphragm was degenerated and necrotic in AOPP rats,Xuebijing injection can lessen the injury in such rats,and the curative effect may be related to the improvement of the Na+-K+-ATPase and Ca2+-ATPsae activities of diaphragm.