CAJ | 학술논문

目的　一系列的研究表明补体激活在心肌损伤中起重要作用。然而，补体激活对心肌的直接损伤作用以及补体介导损伤的机制尚不清楚。本研究评价补体介导的豚鼠离体工作心脏损伤以及CD59对补体介导心肌损伤的保护作用。方法　使用改良的Langendorff灌注装置，以Krebs-Henseleit灌注液灌注离体豚鼠工作心脏，然后分别在灌注液中加入3%灭活人血浆＋酵母多糖（IPZ组，n=10），3%人血浆＋酵母多糖（NPZ组，n=10）和CD59（1.5μg/ml）＋3%正常人血浆＋酵母多糖（NPZC组，n=10），记录各组处理前和处理后15、30、45和60分钟的心率(HR)、心输出量（CO）、冠脉流量（CF）、左心室最大内压（LVP max ）、左室内压最大上升和下降速度（±dp/dt max ）和心外膜心电图，并在实验结束时取左心室心肌组织进行免疫组化检查，观察有无C3a或C5b-9在心肌组织沉积。结果IPZ组处理后心外膜心电图和血流动力学指标均无明显变化。NPZ组工作心脏在处理后15分钟出现心外膜心电图ST段轻度下移，30-60分钟之间ST段变为明显抬高；处理后15-60分钟HR增加，CF、CO、LVP max 、+dp/dt max 和-dp/dt max 下降，这些变化以处理后45分钟最明显。NPZC组上述指标处理前后与IPZ组比较无显著性差异。免疫组化检查：IPZ组未见 C3a 或 C5b-9在心肌沉积；NPZ组可见C3a和C5b-9在心肌沉积；NPZC组可见C3a在心肌沉积，未见C5b-9在心肌沉积。结论　激活的人的补体直接引起离体豚鼠工作心脏损伤，CD59对补体介导的离体豚鼠心脏损伤有保护作用。
목적　일계렬적연구표명보체격활재심기손상중기중요작용。연이，보체격활대심기적직접손상작용이급보체개도손상적궤제상불청초。 본연구평개보체개도적돈서리체공작심장손상이급CD59대보체개도심기손상적보호작용。 방법　사용개량적Langendorff관주장치，이Krebs-Henseleit관주액관주리체돈서공작심장，연후분별재관주액중가입3%멸활인혈장＋효모다당（IPZ조，n=10），3%인혈장＋효모다당（NPZ조，n=10）화CD59（1.5μg/ml）＋3%정상인혈장＋효모다당（NPZC조，n=10），기록각조처리전화처리후15、30、45화60분종적심솔(HR)、심수출량（CO）、관맥류량（CF）、좌심실최대내압（LVP max ）、좌실내압최대상승화하강속도（±dp/dt max ）화심외막심전도，병재실험결속시취좌심실심기조직진행면역조화검사，관찰유무C3a혹C5b-9재심기조직침적。 결과IPZ조처리후심외막심전도화혈류동역학지표균무명현변화。NPZ조공작심장재처리후15분종출현심외막심전도ST단경도하이，30-60분종지간ST단변위명현태고；처리후15-60분종HR증가，CF、CO、LVP max 、+dp/dt max 화-dp/dt max 하강，저사변화이처리후45분종최명현。NPZC조상술지표처리전후여IPZ조비교무현저성차이。면역조화검사：IPZ조미견 C3a 혹 C5b-9재심기침적；NPZ조가견C3a화C5b-9재심기침적；NPZC조가견C3a재심기침적，미견C5b-9재심기침적。 결론　격활적인적보체직접인기리체돈서공작심장손상，CD59대보체개도적리체돈서심장손상유보호작용。
Objective To assess complement-mediated myocardial injury on isolated guinea pig working hearts and cardioprotective effects of CD59. Methods Using a modified Langendorff apparatus, isolated guinea-pig working hearts were perfused with a modified Krebs Henseleit buffer containing 3% heat-inactivated human plasma and zymosan (IPZ) (control) (n=10), 3% normal human plasma and zymosan (NPZ) (n=10), or 3% normal human plasma and zymosan and 1.5μg/ml CD59 (NPZC)(n=10), respectively. Epicardial electrocardiogram (ECG), cardiac output (CO), coronary arterial flow (CF), maximum left ventricular developed pr essure (LVPmax), maximum left ventricular developed pressure increase rate (+dp/dtmax), maximum left ventricular developed pressure decrease rate (- dp/dtmax) and heart rate (HR) were recorded at 0, 15, 30, 45 and 60 min of treatment. After the experiment, immunohistochemical examination was performed to detect the presence of C3a or C5b-9 in the myocardium of the isolated hear ts. Results Compared the IPZ group, hearts treated with NPZ showed a slight depression on ST segments of epicardial ECG at 15 min, a significant elevation between 30min to 60min, a decrease in CF, CO, LVPmax, +dp/dtmax and -dp/dtmax, and an increase in HR at 15 min. The observed alterations in CF, CO, LVPma x, +dp/dtmax and -dp/dtmax remained decreased, while the HR remai ned increased until the end of the protocol. The all above parameters of hearts treated with NPZC were similar to the control group (IPZ) at any given time. I mmunohistochemical examination showed positive signals of C3a and C5b-9 in the myocardium of hearts treated with NPZ. C3a was positive in NPZC, and C3a and C5 b-9 were negative in IPZ. Conclusions Activated human complements directly damage isolated guinea pi g working hearts, and CD59 offers a significant protection against the injuries .