CAJ | 학술논문

目的评价七氟醚后处理对大鼠缺血再灌注心肌细胞胀亡的影响及线粒体通透性转换孔(MPTP)在其中的作用.方法雄性SD大鼠60只,3月龄,体重280 ～ 360 g,采用随机数字表法,将其分为5组(n=12):假手术组(S组)、缺血再灌注组(I/R组)、七氟醚后处理组(SP组)、七氟醚后处理+苍术苷组(SP+ ATR组)和苍术苷组(ATR组).采用结扎左冠状动脉前降支30 min后再灌注的方法制备心肌缺血再灌注模型.SP组和SP+ ATR组于缺血27 min到再灌注开始后2 min吸入2.5％七氟醚,共5 min,其余组吸入氧浓度33％的空气.SP+ ATR组和ATR组于缺血前15 min经颈静脉注射MPTP开放剂苍术苷5 mg/kg.记录心率和收缩压,计算二者乘积(RPP)；于再灌注2h时取心肌组织,测定心肌梗死范围；电镜下观察心肌超微结构；采用Western blot法测定诱导膜损伤的前胀亡受体(Porimin)表达水平；采用分光光度法测定心肌烟酰胺腺嘌呤二核苷酸(NAD+)含量.结果与S组比较,其余4组心肌梗死范围扩大,Porimin表达上调,NAD+含量和RPP降低(P＜0.05)；与I/R组和SP+ATR组比较,SP组心肌梗死范围缩小,Porimin表达下调,NAD+含量升高(P＜0.05),ATR组上述指标差异无统计学意义(P＞0.05).结论七氟醚后处理可通过抑制MPTP开放,减少心肌细胞胀亡,对大鼠缺血再灌注心肌起到保护作用.
목적 평개칠불미후처리대대서결혈재관주심기세포창망적영향급선립체통투성전환공(MPTP)재기중적작용.방법 웅성SD대서60지,3월령,체중280 ～ 360 g,채용수궤수자표법,장기분위5조(n=12):가수술조(S조)、결혈재관주조(I/R조)、칠불미후처리조(SP조)、칠불미후처리+창술감조(SP+ ATR조)화창술감조(ATR조).채용결찰좌관상동맥전강지30 min후재관주적방법제비심기결혈재관주모형.SP조화SP+ ATR조우결혈27 min도재관주개시후2 min흡입2.5％칠불미,공5 min,기여조흡입양농도33％적공기.SP+ ATR조화ATR조우결혈전15 min경경정맥주사MPTP개방제창술감5 mg/kg.기록심솔화수축압,계산이자승적(RPP)；우재관주2h시취심기조직,측정심기경사범위；전경하관찰심기초미결구；채용Western blot법측정유도막손상적전창망수체(Porimin)표체수평；채용분광광도법측정심기연선알선표령이핵감산(NAD+)함량.결과 여S조비교,기여4조심기경사범위확대,Porimin표체상조,NAD+함량화RPP강저(P＜0.05)；여I/R조화SP+ATR조비교,SP조심기경사범위축소,Porimin표체하조,NAD+함량승고(P＜0.05),ATR조상술지표차이무통계학의의(P＞0.05).결론 칠불미후처리가통과억제MPTP개방,감소심기세포창망,대대서결혈재관주심기기도보호작용.
Objective To investigate the effects of sevoflurane postconditioning on myocardial ischemiareperfusion (I/R)-induced oncosis of cardiomyocytes and the role of mitochondrial permeability transition pore (MPTP) in it.Methods Sixty male Sprague-Dawley rats,aged 3 months,weighing 280-360 g,were randomly divided into 5 groups (n =12 each):sham operation group (group S),group I/R,sevoflurane postconditioning group (group SP),sevoflurane postconditioning + atractyloside group (group SP + ATR) and atractyloside group (group ATR).Myocardial ischemia was induced by 30 min occlusion of left anterior descending branch (LAD) of coronary artery followed by 2 h reperfusion.2.5 ％ sevoflurane was inhaled for 5 min starting from 27 min of ischemia until 2 min after beginning of reperfusion in SP and SP + ATR groups,while 33 ％ oxygen was inhaled in the other groups.In SP + ATR and ATR groups,atractyloside 5 mg/kg was injected via the internal jugular vein at 15 min before ischemia.HR and systolic pressure were monitored and recorded and rate-pressure product (RPP) was calculated.At the end of reperfusion,the rats were sacrificed and the hearts removed for determination of myocardial infarct size.The myocardial ultrastrncture was observed by electron microscopy.The expression of Porimin (Pro-oncosis receptor inducing membrane injury) was measured by Western blot.Myocardial nicotinamide adenine dinucleotide (NAD+) content was determined by spectrophotometry.Results Compared with group S,the myocardial infarct size was significantly enlarged,the expression of Porimin was up-regulated,and NAD+ content and RPP were decreased in the other four groups (P ＜ 0.05).Compared with groups I/R and SP + ATR,the infarct size was significantly decreased,the expression of Porimin was down-regulated,and NAD+ content was increased in group SP (P ＜ 0.05),and no significant change was found in the indices mentioned above in group ATR (P ＞0.05).Conclusion Sevoflurane postconditioning can mitigate myocardial I/R injury by inhibiting MPTP opening and reducing oncosis of cardiomyocytes.