国际医药卫生导报
國際醫藥衛生導報
국제의약위생도보
INTERNATIONAL MEDICINE & HEALTH GUIDANCE NEWS
2011年
11期
1286-1290
,共5页
肢体缺血预处理%肢体缺血后处理%无创%缺血/再灌注损伤%心肌保护
肢體缺血預處理%肢體缺血後處理%無創%缺血/再灌註損傷%心肌保護
지체결혈예처리%지체결혈후처리%무창%결혈/재관주손상%심기보호
Limb ischemic preconditioning%Limb ischemic postconditioning%Noninvasive%Ischemia /reperfusion injury%Myocardial protection
目的 探讨无创肢体缺血预处理(NILIPC)和后处理(NILIPostC)联合应用对体外循环心脏手术中心肌缺血/再灌注损伤的保护作用.方法 60例风湿性心脏病拟行机械瓣膜置换者随机分为实验1、2、3组和对照组.实验1组在主动脉阻断前10 min右下肢实施NILIPC;实验2组在主动脉开放前10 min右下肢实施NILIPostC;实验3组在主动脉阻断前10 min右下肢实施NILIPC,主动脉开放前10 min左下肢实施NILIPostC;对照组不施加肢体缺血处理.全组患者于手术前、阻断时、开放时、开放后3 h、12 h、24 h、72 h检测肌钙蛋白Ⅰ(cTnI)和心肌酶肌酸酶同工酶(CK-MB)的血清浓度.结果 主动脉阻断后,各组CK-MB和cTnI均呈上升趋势,于开放后12 h达峰值,其中对照组CK-MB由(21.4±2.95)U/L至(143.9±21.7)U/L,cTnI由0ng/ml至(6.014±1.505)ng/ml,增幅最大;实验3组CK-MB由(19.3 ±4.19)U/L至(86.7±16.3)U/L,cTnI由0 ng/ml至(2.851±0.997)ng/ml,增幅最小.随后下降,实验3组于开放后72 h,CK-MB和cTnI达(25.4±10.8)U/L和(0.399 ±0.107)ng/ml,率先接近术前水平,而实验1、2组和对照组仍明显高于术前(P<0.05.<0.01 ).开放后3 h、12 h、24h、72h,实验3组CK-MB(34.9±23.7、86.7±16.3、56.4±17.9、25.4±10.8)U/L,cTnI(1.008±0.415、2.851±0.997、1.130±0.458、0.399±0.107)ng/ml,与对照组CK-MB(57.2±21.3、143.9±21.7、102.7±23.4、61.9±25.1)U/L,cTnI(1.927±0.971、6.014±1.505、3.985±0.892、1.826±0.973)ng/ml分别比较差异均有统计学意义(P<0.05,<0.01);实验3组与实验1组CK-MB(43.2±18.8、112.8±27.1、85.2±22.3、42.7±19.6)U/L,cTnI(1.283±0.437、4.311±1.084、2.201±0.852、0.917±0.226)ng/ml和实验2组CK-MB(49.6±24.5、121.3±35.2、94.6±28.0、50.2±21.3)U/L、cTnI(1.466±0.539、4.758±1.263、2.164±1.301、1.015±0.271)ng/ml分别比较差异均无统计学意义(P>0.05),但四个时点均数的绝对值却明显低于实验1和2组.结论 在预防体外循环所致的心肌缺血/再灌注损伤中,NILIPC和NILIPostC联合应用可产生加强的心肌保护作用.
目的 探討無創肢體缺血預處理(NILIPC)和後處理(NILIPostC)聯閤應用對體外循環心髒手術中心肌缺血/再灌註損傷的保護作用.方法 60例風濕性心髒病擬行機械瓣膜置換者隨機分為實驗1、2、3組和對照組.實驗1組在主動脈阻斷前10 min右下肢實施NILIPC;實驗2組在主動脈開放前10 min右下肢實施NILIPostC;實驗3組在主動脈阻斷前10 min右下肢實施NILIPC,主動脈開放前10 min左下肢實施NILIPostC;對照組不施加肢體缺血處理.全組患者于手術前、阻斷時、開放時、開放後3 h、12 h、24 h、72 h檢測肌鈣蛋白Ⅰ(cTnI)和心肌酶肌痠酶同工酶(CK-MB)的血清濃度.結果 主動脈阻斷後,各組CK-MB和cTnI均呈上升趨勢,于開放後12 h達峰值,其中對照組CK-MB由(21.4±2.95)U/L至(143.9±21.7)U/L,cTnI由0ng/ml至(6.014±1.505)ng/ml,增幅最大;實驗3組CK-MB由(19.3 ±4.19)U/L至(86.7±16.3)U/L,cTnI由0 ng/ml至(2.851±0.997)ng/ml,增幅最小.隨後下降,實驗3組于開放後72 h,CK-MB和cTnI達(25.4±10.8)U/L和(0.399 ±0.107)ng/ml,率先接近術前水平,而實驗1、2組和對照組仍明顯高于術前(P<0.05.<0.01 ).開放後3 h、12 h、24h、72h,實驗3組CK-MB(34.9±23.7、86.7±16.3、56.4±17.9、25.4±10.8)U/L,cTnI(1.008±0.415、2.851±0.997、1.130±0.458、0.399±0.107)ng/ml,與對照組CK-MB(57.2±21.3、143.9±21.7、102.7±23.4、61.9±25.1)U/L,cTnI(1.927±0.971、6.014±1.505、3.985±0.892、1.826±0.973)ng/ml分彆比較差異均有統計學意義(P<0.05,<0.01);實驗3組與實驗1組CK-MB(43.2±18.8、112.8±27.1、85.2±22.3、42.7±19.6)U/L,cTnI(1.283±0.437、4.311±1.084、2.201±0.852、0.917±0.226)ng/ml和實驗2組CK-MB(49.6±24.5、121.3±35.2、94.6±28.0、50.2±21.3)U/L、cTnI(1.466±0.539、4.758±1.263、2.164±1.301、1.015±0.271)ng/ml分彆比較差異均無統計學意義(P>0.05),但四箇時點均數的絕對值卻明顯低于實驗1和2組.結論 在預防體外循環所緻的心肌缺血/再灌註損傷中,NILIPC和NILIPostC聯閤應用可產生加彊的心肌保護作用.
목적 탐토무창지체결혈예처리(NILIPC)화후처리(NILIPostC)연합응용대체외순배심장수술중심기결혈/재관주손상적보호작용.방법 60례풍습성심장병의행궤계판막치환자수궤분위실험1、2、3조화대조조.실험1조재주동맥조단전10 min우하지실시NILIPC;실험2조재주동맥개방전10 min우하지실시NILIPostC;실험3조재주동맥조단전10 min우하지실시NILIPC,주동맥개방전10 min좌하지실시NILIPostC;대조조불시가지체결혈처리.전조환자우수술전、조단시、개방시、개방후3 h、12 h、24 h、72 h검측기개단백Ⅰ(cTnI)화심기매기산매동공매(CK-MB)적혈청농도.결과 주동맥조단후,각조CK-MB화cTnI균정상승추세,우개방후12 h체봉치,기중대조조CK-MB유(21.4±2.95)U/L지(143.9±21.7)U/L,cTnI유0ng/ml지(6.014±1.505)ng/ml,증폭최대;실험3조CK-MB유(19.3 ±4.19)U/L지(86.7±16.3)U/L,cTnI유0 ng/ml지(2.851±0.997)ng/ml,증폭최소.수후하강,실험3조우개방후72 h,CK-MB화cTnI체(25.4±10.8)U/L화(0.399 ±0.107)ng/ml,솔선접근술전수평,이실험1、2조화대조조잉명현고우술전(P<0.05.<0.01 ).개방후3 h、12 h、24h、72h,실험3조CK-MB(34.9±23.7、86.7±16.3、56.4±17.9、25.4±10.8)U/L,cTnI(1.008±0.415、2.851±0.997、1.130±0.458、0.399±0.107)ng/ml,여대조조CK-MB(57.2±21.3、143.9±21.7、102.7±23.4、61.9±25.1)U/L,cTnI(1.927±0.971、6.014±1.505、3.985±0.892、1.826±0.973)ng/ml분별비교차이균유통계학의의(P<0.05,<0.01);실험3조여실험1조CK-MB(43.2±18.8、112.8±27.1、85.2±22.3、42.7±19.6)U/L,cTnI(1.283±0.437、4.311±1.084、2.201±0.852、0.917±0.226)ng/ml화실험2조CK-MB(49.6±24.5、121.3±35.2、94.6±28.0、50.2±21.3)U/L、cTnI(1.466±0.539、4.758±1.263、2.164±1.301、1.015±0.271)ng/ml분별비교차이균무통계학의의(P>0.05),단사개시점균수적절대치각명현저우실험1화2조.결론 재예방체외순배소치적심기결혈/재관주손상중,NILIPC화NILIPostC연합응용가산생가강적심기보호작용.
Objective To explore the protective effect of noninvasive limb ischemic postconditioning ( NILIPC ) and preconditioning ( MLIPostC ) on ischemia/reperfusion injury during open heart surgery. Methods Sixty patients with rheumatic heart disease scheduled for heart mechanical valve replacement were randomly assigned to study group A , B, or C, or control group (15 patients for each group ). NILIPC or NILIPostC was performed 10 minutes before aorta clamping or off-clamping. Group A received NILIPC and group B received NILIPostC on the right thigh; group C received NILIPC on the right and NILIPostC on the left. The control group received routine treatment. Serum levels of creatine kinase-MB ( CK-MB ) and cardiac troponin-1 (cTnI) were measured preoperatively, at the moment of aorta clamping and off-clamping, and at 3h, 12h, 24h, and 72h after off-clamping. Results Levels of CK-MB and cTnI increased gradually after aorta off-clamping, peaked at 12h, then gradually decreased in all the patients. The control group had a largest increase, while group C had a smallest elevation and declined to the baseline at 72h. At 3h, 12h, 24h, and 72h after aorta off-clamping, levels of CK-MB and cTnI were higher in the control group than in group C ( P< 0.05, P< 0.01 ), but the mean levels of CK-MB and cTnI were lower, as compared with those in groups A and B. Conclusions Combination with NILIPC and NILIPostC may synergically protect myocardium from ischemia/reperfusion injury during open heart surgery.
