CAJ | 학술논문

背景:创伤性休克后,有大量炎性因子、一氧化氮合成、释放,在休克向不可逆的转化过程中起着重要作用.目的:探讨创伤性休克时大鼠血浆肾上腺髓质素(AM)和一氧化氮的变化特点及相关性.设计:随机对照实验研究.地点和材料:实验在第一军医大学珠江医院完成.健康SD大鼠40只,雌雄不拘,质量280～300 g.由第一军医大学实验动物中心提供.干预:将40只SD大鼠分为对照组(10只)、休克未复苏组(10只)、休克复苏组(10只)和氨基胍(Aminoguanidine,AG)组(10只).对照组10只麻醉后插管;30只SD大鼠制作创伤性休克动物模型,双侧股骨干砸伤后并经股动脉放血至MAP35～45 mm Hg.休克复苏组血压维持30 min,然后回输失血和等量的林格氏液.氨基胍组在复苏时静脉注射AG60 mg/kg.观察休克前后血浆AM和一氧化氮浓度的动态变化.主要观察指标:4组大鼠在创伤性休克时AM和一氧化氮的变化及相关性.结果:大鼠创伤性休克后,未复苏组和复苏O.5 h时AM分别为(86.89±2.23)和(43.88±2.74)ng/L达到高峰;一氧化氮浓度分别为(47.88±2.29)和(86.56±2.15)μmol/L,均高于对照组.氨基胍组两指标变化不明显,AM的变化与一氧化氮的变化呈正相关.结论:提示AM与一氧化氮在创伤性休克发生发展中起重要的调节作用,且AM可能是通过一氧化氮介导而发生作用.
배경:창상성휴극후,유대량염성인자、일양화담합성、석방,재휴극향불가역적전화과정중기착중요작용.목적:탐토창상성휴극시대서혈장신상선수질소(AM)화일양화담적변화특점급상관성.설계:수궤대조실험연구.지점화재료:실험재제일군의대학주강의원완성.건강SD대서40지,자웅불구,질량280～300 g.유제일군의대학실험동물중심제공.간예:장40지SD대서분위대조조(10지)、휴극미복소조(10지)、휴극복소조(10지)화안기고(Aminoguanidine,AG)조(10지).대조조10지마취후삽관;30지SD대서제작창상성휴극동물모형,쌍측고골간잡상후병경고동맥방혈지MAP35～45 mm Hg.휴극복소조혈압유지30 min,연후회수실혈화등량적림격씨액.안기고조재복소시정맥주사AG60 mg/kg.관찰휴극전후혈장AM화일양화담농도적동태변화.주요관찰지표:4조대서재창상성휴극시AM화일양화담적변화급상관성.결과:대서창상성휴극후,미복소조화복소O.5 h시AM분별위(86.89±2.23)화(43.88±2.74)ng/L체도고봉;일양화담농도분별위(47.88±2.29)화(86.56±2.15)μmol/L,균고우대조조.안기고조량지표변화불명현,AM적변화여일양화담적변화정정상관.결론:제시AM여일양화담재창상성휴극발생발전중기중요적조절작용,차AM가능시통과일양화담개도이발생작용.
BACKGROUND: Many inflammatory factors and nitric oxide(NO) are synthesized and released in traumatic shock, and play important roles in the process of shock.OBJECTIVE: To investigate the changes and correlation of adrenomedullin (AM) and nitric oxide(NO) in rats with traumatic shock.DESIGN: Randomized and controlled experimental study was adopted.SETTING and MATERIALS: The experiment was completed in Zhujiang Hospital of the First Military Medical University. Forty healthy SD rats, of either gender, weighing 280 - 300 g, were provided by the Experiment Animal Center of the First Military Medical University.INTERVENTION: Fourty Sprague-Dawley(SD) rats were randomly divided into control group(n= 10), traumatic shock without resuscitation group(n=10), traumatic shock on resuscitation group( n = 10) and aminpguandine(AG) group(n=10) . Ten rats as controls received cannulation after anesthesia. Thirty SD rats were made animal models of traumatic shock. Shafts of femurs of both sides were crashed and bled to mean arterial pressure(MAP) of 35 -45 mm Hg via femoral artery. Hypotention of rats in traumatic shock on resuscitation group were maintained 30 minutes,and then the lost blood was returned with an infusion with Ringer' s solution of the equal quantity. Rats of aminpguandine group were injected with aminpguandine 60 mg/kg. Then the changes of Plasma levels of AM and NO were observed.MAIN OUTCOME MEASURES: Changes and correlation of AM and NO after traumatic shock among the rats of the four groups.RESULTS: After the traumatic shock, the peak plasma level of AM at the 0.5 hour time point of the group without resuscitation and the group on resuscitation were (86. 89 ±2.23) and (143.88 ±2.74) ng/L respectively and the levels of NO were (47.88 + 2.29) and (86.56±2.15)μmol/L respectively, which were all higher than those of the control group. Changes were not significant in plasma level of AM and NO in aminpguandine group. The changes of concentration of AM were positively correlated with those of NO.CONCLUSION: AM and NO plays an important role in the pathological process of traumatic shock. The role played by AM in the process is probably through the mediation of NO.