CAJ | 학술논문

目的研究内源性心肌保护机制—缺血预适应（Ischemic-preconditioning，IPC）对未成熟心肌线粒体及能量代谢的影响，并探讨其作用机制。方法采用改良Langendorff-Neely离体鼠心灌流装置，建立未成年大鼠（4周龄）离体心脏顺行灌注左心作功模型。36只大鼠随机等分为缺血对照组（NC）、St.ThomasII晶体停搏液组（ST）、预缺血加停搏液组（PI）。比较再灌注后各组心功能（LVPSP,LVEDP,±dp/dtmax，CO）的恢复率；测定缺血前、再灌注后线粒体游离钙（Ca2+）、丙二醛（MDA）、超氧化物歧化酶（SOD）及心肌ATP含量；观察再灌注后心肌及线粒体超微结构的变化。结果IP组心功能指标的恢复率明显好于ST组和NC组（P<0.05）；再灌注后ST组、NC组心肌线粒体Ca2+、MDA含量明显增高，SOD含量明显减少（P<0.05），而IP组则无明显变化；IP组、ST组ATP含量无显著差别，均明显高于NC组；ST组、NC组心肌及线粒体超微结构破坏明显，IP组则仅有轻微改变。结论St.ThomasII晶体停搏液能减轻未成熟心肌能量损耗，但对心肌线粒体的保护作用较小，影响了收缩功能的恢复；IPC并未增加心肌能量的额外损耗，可明显提高未成熟心肌线粒体的抗氧化能力和钙调节能力，减轻线粒体过氧化损伤和Ca2+超载，维护其正常结构，从而促进收缩功能的恢复。
목적연구내원성심기보호궤제—결혈예괄응（Ischemic-preconditioning，IPC）대미성숙심기선립체급능량대사적영향，병탐토기작용궤제。방법채용개량Langendorff-Neely리체서심관류장치，건립미성년대서（4주령）리체심장순행관주좌심작공모형。36지대서수궤등분위결혈대조조（NC）、St.ThomasII정체정박액조（ST）、예결혈가정박액조（PI）。비교재관주후각조심공능（LVPSP,LVEDP,±dp/dtmax，CO）적회복솔；측정결혈전、재관주후선립체유리개（Ca2+）、병이철（MDA）、초양화물기화매（SOD）급심기ATP함량；관찰재관주후심기급선립체초미결구적변화。결과IP조심공능지표적회복솔명현호우ST조화NC조（P<0.05）；재관주후ST조、NC조심기선립체Ca2+、MDA함량명현증고，SOD함량명현감소（P<0.05），이IP조칙무명현변화；IP조、ST조ATP함량무현저차별，균명현고우NC조；ST조、NC조심기급선립체초미결구파배명현，IP조칙부유경미개변。결론St.ThomasII정체정박액능감경미성숙심기능량손모，단대심기선립체적보호작용교소，영향료수축공능적회복；IPC병미증가심기능량적액외손모，가명현제고미성숙심기선립체적항양화능력화개조절능력，감경선립체과양화손상화Ca2+초재，유호기정상결구，종이촉진수축공능적회복。
Objective To observe the protective effects of ischemicpreconditioning on the mitochondria(Mi)and energy metabolism in immature rat myocardial cells under ischemic condition followed by reperfusion. Methods Isolated working heart models were established using 4-weed-old rats, divided into 3 groups (12 in each group). The control rats (NC group)underwent 120 min of gllobal ischemia followed by 60 min of reperfusion with Krebs-Henseleit(K-H)solution at 37 ℃. The rats subjected to cardioplegic arrest with cold (4 ℃) St.ThomasⅡ Hospital Solution before prolonged global ischemia and reperfusion served as ST group. The rats in ischemic preconditioning group (PI group) was given the same treatment as ST group after 5 min of global ischemia followed by 5 min of reperfusion at 37 ℃ with K-H solution, Malodiadehyde (MDA),free calcium(Ca2+) and superoxide dismutase(SOD) content in the mitochodria and myocardial ATP level were assessed before ischemia and during reperfusion. In addition, the cardiacfunction was measured and changes in the ultrastructures of the myocardial cells observed. Results The recovery of left ventricular function was much better in PI group than in NC and ST groups(P<0.05). MDA and Ca2+ content in the mitochondria were markedly lowered and SOD level elevated in PI group compared with those in the other 2 groups (P<0.05). The myocardial ATP content was markedly higher in PI and ST group. Slight ultrastuctural changes of the mitochondria were observed in IP group,in contrary to the condition observed in NC and ST group. Conclusion ischemic preconditioning may provide protection in addition to the effect of crystollid cardioplegic ischemia on immature myocardium against reperfusion injury.The mechanisms by which ischemic preconditioning protects the myocardium may lie in the decrease of oxgen free radical and Ca2+ overload in the mitochondria and the preservation of ATP as well as the maintance of integration of myocardial and mitochondria ultrastructure.