中华器官移植杂志
中華器官移植雜誌
중화기관이식잡지
CHINESE JOURNAL OF ORGAN TRANSPLANTATION
2009年
8期
451-455
,共5页
杨柳青%喻田%刘兴奎%余志豪
楊柳青%喻田%劉興奎%餘誌豪
양류청%유전%류흥규%여지호
吡那地尔%钾通道%心脏%器官保存
吡那地爾%鉀通道%心髒%器官保存
필나지이%갑통도%심장%기관보존
Pinacidil%Potassium channels%Heart%Organ preservation
目的 观察含钾通道开放剂的供心保存液对心功能以及能量代谢、线粒体呼吸酶活性及超微结构的影响.方法 将SD大鼠分为HTK组、Pi组、5HD组、1098组和5HD+1098组.切取SD大鼠心脏,建立Langendorff灌注模型,平衡10 min,然后按分组进行如下处理:HTK组心脏以Histidine-Tryptophan-Ketoglutarate液(HTK液)停搏;Pi组心脏以含0.5 mmol/L吡那地尔(Pi)的HTK液停搏;1098组心脏以含0.5 mmol/L Pi和100 μmol/L HMR1098的HTK液停搏;5HD组心脏以含0.5 mmol/L Pi和100 μmol/L五羟葵酸(5HD)的HTK液停搏;5HD+1098组心脏以含0.5 μmol/L Pi、100 μmol/L 5HD和100μmol/L HMR1098的HTK液停搏.停搏后,将心脏置于各组相应的液体(4℃)中保存8 h,然后用含氧的37℃克-亨液(K-H液)再灌注60 min.观察各组平衡末、保存末、再灌注末时的心功能、线粒体呼吸酶活性、心肌ATP含量及心肌细胞线粒体超微结构的改变.结果 Pi组保存末、再灌注末的心功能(心率、左心室舒张末压、左心室发展压和冠状动脉流量)、心肌线粒体呼吸酶(NADH氧化酶、琥珀酸氧化酶、细胞色素C氧化酶)活性及ATP含量均优于其他各组(P<0.01或P<0.05),同时线粒体的结构改变也最轻.结论 含Pi的HTK液能改善大鼠心脏保存效果;Pi对能量状态的维持以及对线粒体结构与功能的保护可能是其心肌保护的重要机制.
目的 觀察含鉀通道開放劑的供心保存液對心功能以及能量代謝、線粒體呼吸酶活性及超微結構的影響.方法 將SD大鼠分為HTK組、Pi組、5HD組、1098組和5HD+1098組.切取SD大鼠心髒,建立Langendorff灌註模型,平衡10 min,然後按分組進行如下處理:HTK組心髒以Histidine-Tryptophan-Ketoglutarate液(HTK液)停搏;Pi組心髒以含0.5 mmol/L吡那地爾(Pi)的HTK液停搏;1098組心髒以含0.5 mmol/L Pi和100 μmol/L HMR1098的HTK液停搏;5HD組心髒以含0.5 mmol/L Pi和100 μmol/L五羥葵痠(5HD)的HTK液停搏;5HD+1098組心髒以含0.5 μmol/L Pi、100 μmol/L 5HD和100μmol/L HMR1098的HTK液停搏.停搏後,將心髒置于各組相應的液體(4℃)中保存8 h,然後用含氧的37℃剋-亨液(K-H液)再灌註60 min.觀察各組平衡末、保存末、再灌註末時的心功能、線粒體呼吸酶活性、心肌ATP含量及心肌細胞線粒體超微結構的改變.結果 Pi組保存末、再灌註末的心功能(心率、左心室舒張末壓、左心室髮展壓和冠狀動脈流量)、心肌線粒體呼吸酶(NADH氧化酶、琥珀痠氧化酶、細胞色素C氧化酶)活性及ATP含量均優于其他各組(P<0.01或P<0.05),同時線粒體的結構改變也最輕.結論 含Pi的HTK液能改善大鼠心髒保存效果;Pi對能量狀態的維持以及對線粒體結構與功能的保護可能是其心肌保護的重要機製.
목적 관찰함갑통도개방제적공심보존액대심공능이급능량대사、선립체호흡매활성급초미결구적영향.방법 장SD대서분위HTK조、Pi조、5HD조、1098조화5HD+1098조.절취SD대서심장,건립Langendorff관주모형,평형10 min,연후안분조진행여하처리:HTK조심장이Histidine-Tryptophan-Ketoglutarate액(HTK액)정박;Pi조심장이함0.5 mmol/L필나지이(Pi)적HTK액정박;1098조심장이함0.5 mmol/L Pi화100 μmol/L HMR1098적HTK액정박;5HD조심장이함0.5 mmol/L Pi화100 μmol/L오간규산(5HD)적HTK액정박;5HD+1098조심장이함0.5 μmol/L Pi、100 μmol/L 5HD화100μmol/L HMR1098적HTK액정박.정박후,장심장치우각조상응적액체(4℃)중보존8 h,연후용함양적37℃극-형액(K-H액)재관주60 min.관찰각조평형말、보존말、재관주말시적심공능、선립체호흡매활성、심기ATP함량급심기세포선립체초미결구적개변.결과 Pi조보존말、재관주말적심공능(심솔、좌심실서장말압、좌심실발전압화관상동맥류량)、심기선립체호흡매(NADH양화매、호박산양화매、세포색소C양화매)활성급ATP함량균우우기타각조(P<0.01혹P<0.05),동시선립체적결구개변야최경.결론 함Pi적HTK액능개선대서심장보존효과;Pi대능량상태적유지이급대선립체결구여공능적보호가능시기심기보호적중요궤제.
Objective To investigate the effects of pinacidil on isolated rat hearts preservation,and evaluate the roles of myocardial mitochondrial KATP channel (mitoKATP) and the effects on mitochondria. Methods 120 SD rats were randomly divided into five groups (n = 24, 8 at every moment of stabilization,storage and reperfusion) as follows: (1) the group of HTK solution as the control group,(2) the group of HTK solution containing pinacidil (the Pi group), (3) the group of HTK solution containing pinacidil and 5-hydroxydecanote (5HD, a selective mitochondrial KATP channel blocker, the 5HD group), (4) the group of HTK solution containing pinacidil, Hoechst-Marion-Roussel 1098 (HMR1098, a selective sarcolemmal KATP channel blocker, the 1098 group),and (5) the group of HTK solution containing pinacidil, 5HD and HMR1098 (the 5HD + 1098 group). The Langendorff perfusion models were established. All hearts were arrested with the above-mentioned five preservation solutions in a Langendorff apparatus respectively and subsequently dipped into the same solution for 8 h at 4 ℃ followed by 60 min of reperfusion. The hemodynamics,mitochondrial respiratory function,ATP levels,cardiac troponin Ⅰ release and myocardial uttrastructure were examined. Results Compared with the other groups, heart performance parameters, mitochondria]respiratory enzyme activity and myocardial ATP contents in the Pi group were significantly improved as well as the myocardial mitochondria Flameng score. The protection was almost abolished by the addition of 5HD and moderately decreased by HMR1098. Conclusion Pinacidil may further improve the myocardial protection efficacy of donor heart preservation. Energy status preservation is one of important mechanisms of pinacidil and the effect depends more on mitochondrial than on sarcolemmal potassium adenosine triphosphate channels.
