CAJ | 학술논문

目的：探究apelin-13对离体Wistar大鼠心脏缺血再灌注后的作用效果及机制。方法55只大鼠随机分为五组：正常组（N组）、apelin-13＋正常组（A组）、缺血再灌注组（I-R组）、apelin-13＋缺血再灌注组（A/I-R组）及经典后处理组（I-Post组）。N组持续正常液灌流150 min；apelin组给予含apelin-13（500 nmol/L）正常液持续灌注150 min；I-R组正常液稳定灌流30 min后，结扎前降支30 min，继以正常液再灌注90 min；A/I-R组给予含apelin-13（500 nmol/L）正常液再灌注20 min，继而以正常液灌流70 min；I-Post组再灌注前行经典后处理（30 s再通30 s缺血，共3次循环）。记录分析左心室发展压（LVDP）、再灌注心律失常（RA）、心肌梗死面积、各组 L 型钙通道蛋白α1c亚单位及钠通道蛋白Vα亚单位的表达水平。结果（1）与N组相比，给予apelin后（即A组）LVDP明显增高（P＜0.05），而进行缺血再灌注处理后LVDP均持续下降，但apelin-13及后处理均可减缓其降低，二者对LVDP的影响差异无统计学意义。（2）对RA的影响：A/I-R组较I-R组RA评分降低（P＜0.05），A/I-R组与I-Post组间RA评分差异无统计学意义（P＞0.05）。（3）对心肌梗死面积的影响：A/I-R组心肌梗死面积较I-R组减小（P＜0.05），A/I-R组与I-Post组间心肌梗死面积差异无统计学意义（P＞0.05）。（4）组间心肌钠、钙通道蛋白表达无差异。结论在心肌缺血再灌注时apelin-13可减少再灌注损伤，改善缺血再灌注后心脏泵功能，减少再灌注性心律失常的发生，缩小梗死面积。apelin-13再灌注具有与经典后处理相似作用，但其作用机制并不是通过改变心肌钠、钙通道蛋白的表达来实现的。
목적：탐구apelin-13대리체Wistar대서심장결혈재관주후적작용효과급궤제。방법55지대서수궤분위오조：정상조（N조）、apelin-13＋정상조（A조）、결혈재관주조（I-R조）、apelin-13＋결혈재관주조（A/I-R조）급경전후처리조（I-Post조）。N조지속정상액관류150 min；apelin조급여함apelin-13（500 nmol/L）정상액지속관주150 min；I-R조정상액은정관류30 min후，결찰전강지30 min，계이정상액재관주90 min；A/I-R조급여함apelin-13（500 nmol/L）정상액재관주20 min，계이이정상액관류70 min；I-Post조재관주전행경전후처리（30 s재통30 s결혈，공3차순배）。기록분석좌심실발전압（LVDP）、재관주심률실상（RA）、심기경사면적、각조 L 형개통도단백α1c아단위급납통도단백Vα아단위적표체수평。결과（1）여N조상비，급여apelin후（즉A조）LVDP명현증고（P＜0.05），이진행결혈재관주처리후LVDP균지속하강，단apelin-13급후처리균가감완기강저，이자대LVDP적영향차이무통계학의의。（2）대RA적영향：A/I-R조교I-R조RA평분강저（P＜0.05），A/I-R조여I-Post조간RA평분차이무통계학의의（P＞0.05）。（3）대심기경사면적적영향：A/I-R조심기경사면적교I-R조감소（P＜0.05），A/I-R조여I-Post조간심기경사면적차이무통계학의의（P＞0.05）。（4）조간심기납、개통도단백표체무차이。결론재심기결혈재관주시apelin-13가감소재관주손상，개선결혈재관주후심장빙공능，감소재관주성심률실상적발생，축소경사면적。apelin-13재관주구유여경전후처리상사작용，단기작용궤제병불시통과개변심기납、개통도단백적표체래실현적。
Objective To observe the effects and mechanism of apelin-13 to ischemia reperfusion through establishing Langendorff rats model. Methods Wistar male rats were randomly divided into 5 groups: normal group (N), apelin-13 group (A), ischemia reperfusion group (I-R), apelin-13+I-R group (A/I-R) and classical ischemia post conditioning group (I-post C). N group: continued perfusion for 150 min with KH liquid. A group:continued perfusion for 150 min with KH liquid containing Apelin-13 (500 nmol/L). I-R group:stable perfusion for 30 min followed by ligating LAD 30 min, then reperfusion for 90 min. A/I-R group:reperfusion with apelin-13 (500 nmol/L) for 20 min. Then perfused with KH liquid for 70 min. I-post C group: I-Post C (reperfusion for 30 s, ligation for 30 s, and 3 cycles in all) before reperfusion. Recorded and observed RA, LVDP by 16 physiological recorder and calculated myocardial infarct size. Observed the expression of myocardial Na+ channel protein and voltage-gated Ca2+ channel protein with Western blot. Results About the LVDP: compared with N group, LVDP was significantly increased in apelin-13 administration group (A group)(P<0.05), but a steady decline was arisen in groups which treated with I-R. The depression was attenuated by apelin-13 and I-Post C. A/I-R and I-Post C grouphad no significant difference in LVDP at the same time (P>0.05). About RA score:RA score in A/I-R group was lower than I-R group (P<0.05), A/I-R and I-Post C group had no significant difference in RA score (P>0.05). About myocardial infarct size: myocardial infarct size in A/I-R was smaller than I-R group (37.45±3.53 vs. 54.27±3.88, P<0.05), A/I-R and I-Post C group had no significant difference in myocardial infarct area (P>0.05). The expression of myocardial Na+channel protein and voltage-gated Ca2+channel protein had no significant difference (P>0.05). Conclusions Apelin-13 has the positive inotropic effect on the myocardium. Apelin-13 can reduce myocardial ischemia reperfusion injury, improve cardiac pump function, reduce the incidence of RA, and decrease infarct area. In addition, the effect of apelin-13 on myocardial ischemia reperfusion injury is similar to I-Post C. The mechanism of apelin-13 to reduce the myocardial ischemia reperfusion injury is not by changing the expression of myocardial Na+ channel protein and voltage-gated Ca2+channel protein.