中华胸心血管外科杂志
中華胸心血管外科雜誌
중화흉심혈관외과잡지
Chinese Journal of Thoracic and Cardiovascular Surgery
2011年
4期
221-223
,共3页
廖健毅%徐洪军%冉旭东%曹鼎方
廖健毅%徐洪軍%冉旭東%曹鼎方
료건의%서홍군%염욱동%조정방
心肺转流术%心脏缺损,先天性%细胞保护%血管内皮细胞%阿魏酸钠
心肺轉流術%心髒缺損,先天性%細胞保護%血管內皮細胞%阿魏痠鈉
심폐전류술%심장결손,선천성%세포보호%혈관내피세포%아위산납
Cardiopulmonary bypass%Heart diseases,congenital%Cytoprotection%Vascular endothelial cells%Sodium%Ferulate
目的 观察婴幼儿先天性心脏病心肺转流术(CPB)围手术期一氧化氮(NO)、内皮素(ET-1)和循环内皮细胞(CEC)水平的变化,初步探讨阿魏酸钠对血管内皮功能的保护作用.方法 60例先天性心脏病病儿随机分为阿魏酸钠组(S组)和对照组(C组)各30例.S组于体外循环前静脉滴注阿魏酸钠注射液8 mg/kg,C组予等量平衡盐溶液,检测CPB前(TO)、30 min(T1)、结束时(T2)、手术后2h(T3)、6 h(T4)5个时间点血浆NO和ET浓度,以及T0和T2两个时间点的CEC变化.结果 两组间T0比较差异不明显,12与T0比较CEC浓度均升高明显;T2时与C组比较,S组CEC升高幅度明显被抑制,差异有统计学意义(P<0.05).两组血浆N0浓度T1均降低,差异有统计学意义,组间比较无统计学意义(P>0.05),T2、T3、T4时间点两组NO浓度均有所上升,但均低于T0,差异明显,S组NO降低程度比C组小(P<0.05).两组T1时ET-1稍有降低,随后ET-1升高明显(P<0.01);S组T1、T2、T3、T4时间点均低于C组,差异有统计学意义(P<0.05或P<0.01).结论 体外循环手术可造成NO/ET失平衡状态,CEC数明显增加,证实CPB后存在着血管内皮功能的损伤.阿魏酸钠组术后NO下降幅度,ET、CEC升高的幅度,明显较对照组小,阿魏酸钠可有效拮抗ET的分泌,促进NO的生成,对婴幼儿体外循环手术有较好的血管内皮功能保护作用.
目的 觀察嬰幼兒先天性心髒病心肺轉流術(CPB)圍手術期一氧化氮(NO)、內皮素(ET-1)和循環內皮細胞(CEC)水平的變化,初步探討阿魏痠鈉對血管內皮功能的保護作用.方法 60例先天性心髒病病兒隨機分為阿魏痠鈉組(S組)和對照組(C組)各30例.S組于體外循環前靜脈滴註阿魏痠鈉註射液8 mg/kg,C組予等量平衡鹽溶液,檢測CPB前(TO)、30 min(T1)、結束時(T2)、手術後2h(T3)、6 h(T4)5箇時間點血漿NO和ET濃度,以及T0和T2兩箇時間點的CEC變化.結果 兩組間T0比較差異不明顯,12與T0比較CEC濃度均升高明顯;T2時與C組比較,S組CEC升高幅度明顯被抑製,差異有統計學意義(P<0.05).兩組血漿N0濃度T1均降低,差異有統計學意義,組間比較無統計學意義(P>0.05),T2、T3、T4時間點兩組NO濃度均有所上升,但均低于T0,差異明顯,S組NO降低程度比C組小(P<0.05).兩組T1時ET-1稍有降低,隨後ET-1升高明顯(P<0.01);S組T1、T2、T3、T4時間點均低于C組,差異有統計學意義(P<0.05或P<0.01).結論 體外循環手術可造成NO/ET失平衡狀態,CEC數明顯增加,證實CPB後存在著血管內皮功能的損傷.阿魏痠鈉組術後NO下降幅度,ET、CEC升高的幅度,明顯較對照組小,阿魏痠鈉可有效拮抗ET的分泌,促進NO的生成,對嬰幼兒體外循環手術有較好的血管內皮功能保護作用.
목적 관찰영유인선천성심장병심폐전류술(CPB)위수술기일양화담(NO)、내피소(ET-1)화순배내피세포(CEC)수평적변화,초보탐토아위산납대혈관내피공능적보호작용.방법 60례선천성심장병병인수궤분위아위산납조(S조)화대조조(C조)각30례.S조우체외순배전정맥적주아위산납주사액8 mg/kg,C조여등량평형염용액,검측CPB전(TO)、30 min(T1)、결속시(T2)、수술후2h(T3)、6 h(T4)5개시간점혈장NO화ET농도,이급T0화T2량개시간점적CEC변화.결과 량조간T0비교차이불명현,12여T0비교CEC농도균승고명현;T2시여C조비교,S조CEC승고폭도명현피억제,차이유통계학의의(P<0.05).량조혈장N0농도T1균강저,차이유통계학의의,조간비교무통계학의의(P>0.05),T2、T3、T4시간점량조NO농도균유소상승,단균저우T0,차이명현,S조NO강저정도비C조소(P<0.05).량조T1시ET-1초유강저,수후ET-1승고명현(P<0.01);S조T1、T2、T3、T4시간점균저우C조,차이유통계학의의(P<0.05혹P<0.01).결론 체외순배수술가조성NO/ET실평형상태,CEC수명현증가,증실CPB후존재착혈관내피공능적손상.아위산납조술후NO하강폭도,ET、CEC승고적폭도,명현교대조조소,아위산납가유효길항ET적분비,촉진NO적생성,대영유인체외순배수술유교호적혈관내피공능보호작용.
Objective Cardiopulmonary bypass (CPB) and its related ischemia reperfusion injury may cause endothelial cell injury.To study the protective effects of sodium ferulate in vascular endothelial function during CPB by testing the changes of vascular endothelial cell( CEC),nitric oxide( NO) and endothelin-1 ( ET-1 ) in children with congenital heart disease.Methods Sixty patients with congenital heart disease,including 28 males and 32 females were studied.The mean age was (19.7 ±10.4) months and body weight (10.5 ±6.1) kg.There were 37 VSD,8 ASD,7 TOF,5 TAPVC and 3 CAVC,among them 26 patients had pulmonary hypertension.They were randomly divided in to two groups:sodium ferulate group ( group S,n = 30),and control group ( group C,n =30) .Sodium ferulate (8 mg/kg) was given intravenously before CPB.Blood samples were taken from the arterial line at following time points:before CPB (TO),bypass 30 min(Tl ),the termination of CPB (T2 ),2h after operation ( T3 ) and 6h after operation ( T4 ),respectively for determination the concentration of vascular endothelial cell (CEC) in the blood,the concentration of nitric oxide (NO) and endothelin-1 ( ET-1) in the plasma.Results There were no significant difference for the two groups regarding above parameters at TO ( P > 0.05).The level of CEC was significantly elevated after CPB in both groups ( P < 0.05 ) .CEC were lower at T2 in group S than in group C ( P < 0.05 ) .NO was decreased in both groups,but was higher in group S at T2,T3 and T4 ( P < 0.05 ) .The concentration of plasma ET-1 was not significantly different before CPB,but there was a slight decrease at T1,and then it was significantly increased in both groups (P<0.05).But it was lower in group S than in group C at T1,T2,T3 and T4(P<0.05 orP<0.01).Conclusion There was severe endothelial cell damage during CPB.Sodium Ferulate can effectively antagonize the secretion of ET-1 to promote the formation of NO.Therefore,it reduces CPB-induced endothelial cell damage and protects vascular endothelial function during CPB.