CAJ | 학술논문

目的探讨吸入一氧化氮(NO)对婴幼儿危重先天性心脏病(先心病)体外循环术(CPB)中肺表面活性物质的影响.方法将30例室间隔缺损伴重度肺动脉高压的婴幼儿随机分为对照组和NO组,NO组在CPB期间吸入40×10-6NO.CPB前和术后气管插管未拔前0～1 h,1～2 h,2～3 h测定气道压、吸入氧浓度和呼气末二氧化碳浓度,并分别在同时点采动脉血进行血气分析,计算肺泡死腔率(VDhD/VT)、肺泡动脉血氧分压差[P(A-a)O2]、动脉血氧含量(CaO2)和肺泡氧合指数(OI),记录术后呼吸机支持时间.同时各时相点以少量生理盐水灌洗气道,分别测定气道吸出物中总磷脂(TPL)、饱和卵磷脂(SatPC)、总蛋白(TP)值,计算SatPC/TPL和SatPC/TP.结果与对照组相比,NO组VD/VTP(A-a)O2明显下降(P<0.01),OI、CaO2升高(P<0.01);两组CPB后SatPC/TPL和SatPC/TP较CPB前明显降低(P<0.01).NO组SatPC/TPL和SatPC/TP下降的幅度明显小于对照组(P<0.01).结论婴幼儿危重先心病CPB中存在明显的肺损害,表现为一些亚临床性肺功能损伤.吸入一定浓度的NO对CPB期间肺功能有保护作用.
목적 탐토흡입일양화담(NO)대영유인위중선천성심장병(선심병)체외순배술(CPB)중폐표면활성물질적영향.방법 장30례실간격결손반중도폐동맥고압적영유인수궤분위대조조화NO조,NO조재CPB기간흡입40×10-6NO.CPB전화술후기관삽관미발전0～1 h,1～2 h,2～3 h측정기도압、흡입양농도화호기말이양화탄농도,병분별재동시점채동맥혈진행혈기분석,계산폐포사강솔(VDhD/VT)、폐포동맥혈양분압차[P(A-a)O2]、동맥혈양함량(CaO2)화폐포양합지수(OI),기록술후호흡궤지지시간.동시각시상점이소량생리염수관세기도,분별측정기도흡출물중총린지(TPL)、포화란린지(SatPC)、총단백(TP)치,계산SatPC/TPL화SatPC/TP.결과 여대조조상비,NO조VD/VTP(A-a)O2명현하강(P<0.01),OI、CaO2승고(P<0.01);량조CPB후SatPC/TPL화SatPC/TP교CPB전명현강저(P<0.01).NO조SatPC/TPL화SatPC/TP하강적폭도명현소우대조조(P<0.01).결론 영유인위중선심병CPB중존재명현적폐손해,표현위일사아림상성폐공능손상.흡입일정농도적NO대CPB기간폐공능유보호작용.
Objective To study the effects of inhale nitric oxide(NO) on pulmonary surfactant during cardiopulmonary bypass(CPB) in infants with severe CHD. Methods Thirty infants with severe CHD were randomly divided into two groups:control group(n=15) and NO group(n=15). Before CPB and after operation 0～1 h, 1～2 h,2～3 h, the cases of NO group had been inhaled 40×10-6 NO till the operation finished. We monitored the followings:mean pulmonary arterial pressure, fractional concentration of inspired oxygen ,end-tidal CO2, the value of volume of dead air space/ tidal volume (VD/VT ), oxygen index (OI), alveolar-arterial PO2 difference[ P(A-a)O2] and oxygen content in arterial blood( CaO2 ). Meanwhile branchoalveolar lavage fluid in each phase point were collected to analyse,the levels of TPL,SatPC,TP were determined and the value of SatPC/TPL and SatPC/TP were calculated. Results The VD/VT P(A-a) O2 in control group were much higher than those in NO group, OI and CaO2 in NO group were higher than those in control group(P<0.01 ). The levels of SatPC/TPL and SatPC/TP at post-operation were lower than those before CPB (P<0.01), and the decreases of SatPC/TPL and SatPC/TP in control group were more than those in NO group. Conclusion Lung ischemia-reperfusion injury was observed obviously during CPB in infants with severe CHD, which manifestes subclinical pulmonary function injury. Inhaled NO has protective effects on lung during CPB in infants with severe CHD.