CAJ | 학술논문

目的研究内源性一氧化碳( CO )在心肺复苏( CPR )后大鼠心肌氧化应激损伤中的变化,并探讨心肌氧化应激损伤是否与内源性CO及血红素加氧酶-1 ( HO-1 )表达相关. 方法将32只雄性SD大鼠随机分为假手术组( Sham组) ,复苏后1 h组( ROSC 1 h组) ,复苏后3 h组( ROSC 3 h组) ,复苏后24 h组( ROSC 24 h组). Sham组只进行手术操作,不进行致颤及CPR.其余三组大鼠均诱导8 min室颤及6 min CPR. 检测各组大鼠心功能、血清CK-MB、心肌组织活性氧( ROS)及丙二醛( MDA)水平;观察心肌组织CO水平、心肌HO-1蛋白水平及HO-1 mRNA表达;分析CPR后大鼠心肌氧化应激损伤与心肌CO水平、HO-1表达的相关性. 结果与Sham组比较,ROSC 1 h组、3 h组及24 h组心功能损伤明显,血清CK-MB水平提高(P<0.05). 大鼠ROSC 1 h组及3 h组心肌ROS及MDA水平均明显高于Sham组( P<0.01);ROSC 24 h组心肌MDA水平高于Sham组(P<0.01). ROSC 1 h组和3 h组心肌组织CO水平、HO-1蛋白水平及HO-1 mRNA水平较Sham组升高明显(P<0.01). ROSC 24 h组心肌CO及HO-1蛋白水平明显高于Sham组(P<0.05). 相关性分析结果显示,CPR后心肌组织CO水平与心肌组织HO-1蛋白的表达及HO-1 mRNA水平呈正相关(P<0.01);心肌组织MDA水平与心肌组织CO水平、HO-1蛋白表达及HO-1 mRNA水平均呈正相关( P<0 .01 );心肌组织ROS水平则与心肌组织CO水平及心肌组织HO-1 mRNA水平呈正相关(P<0.01). 结论室颤大鼠CPR后心肌内源性CO水平及心肌HO-1表达可明显增加,与复苏后心肌氧化应激损伤水平呈明显正相关. 复苏后过度ROS的产生可能是CO及HO-1水平上调的诱发因素之一.
목적 연구내원성일양화탄( CO )재심폐복소( CPR )후대서심기양화응격손상중적변화,병탐토심기양화응격손상시부여내원성CO급혈홍소가양매-1 ( HO-1 )표체상관. 방법 장32지웅성SD대서수궤분위가수술조( Sham조) ,복소후1 h조( ROSC 1 h조) ,복소후3 h조( ROSC 3 h조) ,복소후24 h조( ROSC 24 h조). Sham조지진행수술조작,불진행치전급CPR.기여삼조대서균유도8 min실전급6 min CPR. 검측각조대서심공능、혈청CK-MB、심기조직활성양( ROS)급병이철( MDA)수평;관찰심기조직CO수평、심기HO-1단백수평급HO-1 mRNA표체;분석CPR후대서심기양화응격손상여심기CO수평、HO-1표체적상관성. 결과 여Sham조비교,ROSC 1 h조、3 h조급24 h조심공능손상명현,혈청CK-MB수평제고(P<0.05). 대서ROSC 1 h조급3 h조심기ROS급MDA수평균명현고우Sham조( P<0.01);ROSC 24 h조심기MDA수평고우Sham조(P<0.01). ROSC 1 h조화3 h조심기조직CO수평、HO-1단백수평급HO-1 mRNA수평교Sham조승고명현(P<0.01). ROSC 24 h조심기CO급HO-1단백수평명현고우Sham조(P<0.05). 상관성분석결과현시,CPR후심기조직CO수평여심기조직HO-1단백적표체급HO-1 mRNA수평정정상관(P<0.01);심기조직MDA수평여심기조직CO수평、HO-1단백표체급HO-1 mRNA수평균정정상관( P<0 .01 );심기조직ROS수평칙여심기조직CO수평급심기조직HO-1 mRNA수평정정상관(P<0.01). 결론 실전대서CPR후심기내원성CO수평급심기HO-1표체가명현증가,여복소후심기양화응격손상수평정명현정상관. 복소후과도ROS적산생가능시CO급HO-1수평상조적유발인소지일.
Objective To investigate the variation of endogenous carbon monoxide (CO) and the correlation between endogenous CO , CO -related heme oxygenase -1 ( HO -1 ) expression and myocardial oxidative stress in post resuscitation myocardial injury .Methods Thirty-two male SD rats were randomly assigned into Sham group , restoration of spontaneous circulation ( ROSC) -1 h group, ROSC-3 h group, ROSC-24 h group.Animals in the Sham group were instrumented without cardiac arrest and resuscitation . Animals in other three groups were resuscitated after 8 min ventricular fibrillation and 6min cardiopulmonary resuscitation . Myocardial function , serum CK -MB level, myocardial ROS production , malondialdehyde ( MDA ) and CO level in myocardial tissue were determined.Meanwhile, the content of CO -related HO-1 protein and HO -1 mRNA in myocardial tissue were also examined.Finally, we analyzed the correlation between endogenous CO , CO-relatedHO -1 expression and myocardial oxidative stress . Results Significantly decreased myocardial performance and serum CK -MB level were observed in ROSC -1 h group, ROSC -3 h group and ROSC-24 h group compared with Sham group (P<0.05).The levels of ROS and MDA in cardiac tissue were increased in ROSC -1 h group and ROSC -3 h group compared with Sham group ( P<0.01 ) .The cardiac MDA level was also improved in ROSC -24 h group compared with Sham group (P<0.01).Meanwhile, The levels of CO, HO-1 protein and HO -1 mRNA in myocardial tissue were higher in ROSC -1 h group and ROSC -3 h group than those in Sham group (P<0.01).In ROSC-24 h group, the levels of CO and HO -1 protein were also improved compared with those in Sham group ( P<0.05).After ROSC, the levels of CO were positively correlated with the levels of HO-1 protein and HO-1 mRNA expression (P<0.01).The levels of MDA were positively correlated with the levels of CO, HO-1 protein and HO-1 mRNA (P<0.01).The cardiac ROS levels were also positively correlated with the levels of CO and HO -1 mRNA (P<0.01).Conclusion After ROSC, the levels of CO and HO -1 in cardiac tissue were significantly improved positively correlated with the increased levels of MDA and ROS .Cardiac oxidative stress may induce the increased levels of CO and HO-1 expression.