中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2010年
12期
1431-1434
,共4页
史春霞%李立环%姚允泰%王欣%宋民%于存涛%阮英卯
史春霞%李立環%姚允泰%王訢%宋民%于存濤%阮英卯
사춘하%리립배%요윤태%왕흔%송민%우존도%원영묘
麻醉药,吸入%心肌再灌注损伤%心肺转流术
痳醉藥,吸入%心肌再灌註損傷%心肺轉流術
마취약,흡입%심기재관주손상%심폐전류술
Anesthetics,inhalation%Myocardial reperfusion injury%Cardiopulmonary bypass
目的 探讨七氟醚后处理对体外循环(CPB)下冠状动脉旁路移植术病人心肌缺血再灌注损伤的影响.方法 择期行冠状动脉旁路移植术病人40例,性别不限,年龄55~64岁,BMI<30 kg/m2,NYHA心功能分级Ⅰ~Ⅲ级,随机分为2组(n=20):对照组(C组)和七氟醚后处理组(S组).S组于主动脉开放即刻通过体外循环机吸入2%七氟醚,持续15 min,C组不给予任何处理.分别于麻醉诱导后、CPB转流前、停机后10 min、术毕、术后6和24 h时,记录MAP、HR、CVP、平均肺动脉压、肺动脉楔压、CO和S(v)O2,计算CI、SVI、体循环血管阻力指数和肺循环血管阻力指数.分别于主动脉阻断前、复灌6 h和术后24 h时,中心静脉取血样,测定血浆肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)和乳酸脱氢酶(LDH)的活性以及肌钙蛋白I(TnI)浓度.分别于主动脉阻断前和CPB停机时,取右心耳心肌组织,观察心肌细胞超微结构,并对心肌细胞损伤程度进行评分.结果 两组间各时点血液动力学和心功能指标比较差异无统计学意义(P>0.05).与C组比较,S组复灌6 h时血浆CK-MB和LDH活性降低,术后24 h时血浆CK活性和TnI浓度降低,CPB停机后心肌细胞损伤程度评分降低(P<0.05).结论 七氟醚后处理可减轻CPB下冠状动脉旁路移植术病人心肌缺血再灌注损伤.
目的 探討七氟醚後處理對體外循環(CPB)下冠狀動脈徬路移植術病人心肌缺血再灌註損傷的影響.方法 擇期行冠狀動脈徬路移植術病人40例,性彆不限,年齡55~64歲,BMI<30 kg/m2,NYHA心功能分級Ⅰ~Ⅲ級,隨機分為2組(n=20):對照組(C組)和七氟醚後處理組(S組).S組于主動脈開放即刻通過體外循環機吸入2%七氟醚,持續15 min,C組不給予任何處理.分彆于痳醉誘導後、CPB轉流前、停機後10 min、術畢、術後6和24 h時,記錄MAP、HR、CVP、平均肺動脈壓、肺動脈楔壓、CO和S(v)O2,計算CI、SVI、體循環血管阻力指數和肺循環血管阻力指數.分彆于主動脈阻斷前、複灌6 h和術後24 h時,中心靜脈取血樣,測定血漿肌痠激酶(CK)、肌痠激酶同工酶(CK-MB)和乳痠脫氫酶(LDH)的活性以及肌鈣蛋白I(TnI)濃度.分彆于主動脈阻斷前和CPB停機時,取右心耳心肌組織,觀察心肌細胞超微結構,併對心肌細胞損傷程度進行評分.結果 兩組間各時點血液動力學和心功能指標比較差異無統計學意義(P>0.05).與C組比較,S組複灌6 h時血漿CK-MB和LDH活性降低,術後24 h時血漿CK活性和TnI濃度降低,CPB停機後心肌細胞損傷程度評分降低(P<0.05).結論 七氟醚後處理可減輕CPB下冠狀動脈徬路移植術病人心肌缺血再灌註損傷.
목적 탐토칠불미후처리대체외순배(CPB)하관상동맥방로이식술병인심기결혈재관주손상적영향.방법 택기행관상동맥방로이식술병인40례,성별불한,년령55~64세,BMI<30 kg/m2,NYHA심공능분급Ⅰ~Ⅲ급,수궤분위2조(n=20):대조조(C조)화칠불미후처리조(S조).S조우주동맥개방즉각통과체외순배궤흡입2%칠불미,지속15 min,C조불급여임하처리.분별우마취유도후、CPB전류전、정궤후10 min、술필、술후6화24 h시,기록MAP、HR、CVP、평균폐동맥압、폐동맥설압、CO화S(v)O2,계산CI、SVI、체순배혈관조력지수화폐순배혈관조력지수.분별우주동맥조단전、복관6 h화술후24 h시,중심정맥취혈양,측정혈장기산격매(CK)、기산격매동공매(CK-MB)화유산탈경매(LDH)적활성이급기개단백I(TnI)농도.분별우주동맥조단전화CPB정궤시,취우심이심기조직,관찰심기세포초미결구,병대심기세포손상정도진행평분.결과 량조간각시점혈액동역학화심공능지표비교차이무통계학의의(P>0.05).여C조비교,S조복관6 h시혈장CK-MB화LDH활성강저,술후24 h시혈장CK활성화TnI농도강저,CPB정궤후심기세포손상정도평분강저(P<0.05).결론 칠불미후처리가감경CPB하관상동맥방로이식술병인심기결혈재관주손상.
Objective To investigate the effects of sevoflurane postconditioning on myocardial ischemiareperfusion(I/R)injury in patients undergoing coronary artery bypass grafting(CABG)with cardiopulmonary bypass(CPB).Methods Forty NYHA Ⅰ -Ⅲ patients of both sexes,aged 55-64 yr,with BMI < 30 kg/m2,scheduled for CABG under CPB,were randomly divided into 2 groups(n = 20): control group(group C)and sevoflurane postconditioning group(group S).Anesthesia was induced with midazolam and/or etomidate,fentanyl and rocuronium.Patients were tracheal intubated and mechanically ventilated.Anesthesia was maintained with iv infusion of propefol and intermittent iv injection of fentanyl and pipecuronium.In group S,2% sevoflurane was inhaled continuously for 15 min immediately after aortic unclamping.After anesthesia induction,before CPB,10 min after the end of CPB,at the end of operation,and 6 and 24 h after operation,MAP,HR,CVP,mean pulmonary arterial pressure,pulmonary arterial wedge pressure,CO and S(v)O2 were recorded,and CI,SVI,systemic vascular resistance index and pulmonary vascular resistance index were calculated.Blood samples were taken from central vein before aortic clamping,at 6 h of reperfusion and 24 h after operation for determination of plasma creatine kinase(CK),creatine kinase isoenzyme(CK- M B)and lactate dehydrogenase(LDH)activities and tropenin I(TnI)concentrations.Myocardial tissues were obtained from right auricle before aortic clamping and at the end of CPB for observation of the ultrastructure and the severity of myocardial injury was assessed.Results There was no significant difference in hemodynamics and parameters of cardiac function between the two groups(P > 0.05).Compared with group C,plasma CK-MB and LDH activities at 6 h of reperfusion and plasma CK activity and TnI concentrations at 24 h after operation were significantly decreased and the myocardial injury was significantly reduced after the end of CPB in group S(P < 0.05).Conclusion Sevoflurane postconditioning can protect myocardium against I/R injury induced by CPB in patients undergoing CABG.