CAJ | 학술논문

目的观察上胸段硬膜外阻滞对大鼠心肌梗死后心室重构和心功能的影响,并探讨其机制.方法模型成功的大鼠随机分为假手术组(S组,n=12)、心力衰竭组(CHF组,n=24)和硬膜外阻滞组(HTEA组,n=24).硬膜外置管术后24 h S组和CHF组于硬膜外腔注入9 g/L生理盐水(100μl/kg,2次/d,连续4周).HTEA组于硬膜外腔注入1.25 g/L布比卡因(100 μl/kg,2次/d,连续4周).4周后行超声心动图测定左室舒张末期内径(LVEDD)、左室收缩末期内径(LVESD)左室射血分数(LVEF)和左室短轴缩短率(LVES);测量心脏和左心室质量,计算心脏指数(HW/BW)和左心室指数(LVW/BW);左室心肌组织HE和Masson染色;RT-PCR测定左室心肌β_3AR和eNOSmRNA;免疫组织化学检测左室心肌β_33AR表达.结果 LVEDD和LVESD:HTEA组较CHF组明显缩小(P<0.01);LVEF和LVFS:HTEA组较CHF组明显增加(P<0.05).HW/BW和LVW/BW:CHF组和HTEA组均明显大于s组(P<0.01),但HTEA组较CHF组明显减小(P<0.01).心肌病理学形态学显示:CHF组心肌细胞变性、萎缩,心肌纤维紊乱、断裂,胶原纤维明显增多,HTEA组心肌细胞变性明显减少,非梗死区心肌纤维化明显改善;与CHF组相比,HTEA组β_3AR和eNOS mRNA表达明显减少(P<0.01).结论 HTEA治疗可以改善或减缓急性心肌梗死后大鼠的左室重构和心功能,可能与其下调β_AR表达有关.
목적 관찰상흉단경막외조체대대서심기경사후심실중구화심공능적영향,병탐토기궤제.방법 모형성공적대서수궤분위가수술조(S조,n=12)、심력쇠갈조(CHF조,n=24)화경막외조체조(HTEA조,n=24).경막외치관술후24 h S조화CHF조우경막외강주입9 g/L생리염수(100μl/kg,2차/d,련속4주).HTEA조우경막외강주입1.25 g/L포비잡인(100 μl/kg,2차/d,련속4주).4주후행초성심동도측정좌실서장말기내경(LVEDD)、좌실수축말기내경(LVESD)좌실사혈분수(LVEF)화좌실단축축단솔(LVES);측량심장화좌심실질량,계산심장지수(HW/BW)화좌심실지수(LVW/BW);좌실심기조직HE화Masson염색;RT-PCR측정좌실심기β_3AR화eNOSmRNA;면역조직화학검측좌실심기β_33AR표체.결과 LVEDD화LVESD:HTEA조교CHF조명현축소(P<0.01);LVEF화LVFS:HTEA조교CHF조명현증가(P<0.05).HW/BW화LVW/BW:CHF조화HTEA조균명현대우s조(P<0.01),단HTEA조교CHF조명현감소(P<0.01).심기병이학형태학현시:CHF조심기세포변성、위축,심기섬유문란、단렬,효원섬유명현증다,HTEA조심기세포변성명현감소,비경사구심기섬유화명현개선;여CHF조상비,HTEA조β_3AR화eNOS mRNA표체명현감소(P<0.01).결론 HTEA치료가이개선혹감완급성심기경사후대서적좌실중구화심공능,가능여기하조β_AR표체유관.
Objective To investigate the effect of high thoracic epidural anesthesia on ventricular remodeling and cardiac function in rats with heart failure induced by myocardial infarction, and to investigate their mechanism. Methods Rats that had been established successively model were randomly divided into S group (n = 12) , HTEA group and CHF group (24/group). 9. 0 g/L normal sodium 100 μl/kg was injected to epidural cavity twice a day separately in group S and group CHF. 1. 25 g/L bupivacaine 100 μl/kg was injected to epidural cavity twice a day in group HTEA. Epidural injection was started 24 hrs after the epidural surgery and continued 4 weeks. Then the change of cardiac function was observed by using echocardiogram. The ratio of heart weight to body weight ( HW/BW ) and the ratio of left ventricular weight to body weight (LVW/BW) were measured. Noninfarct ventricular tissue were stained with hematoxylin-eosin (HE) and Masson's trichrome respectively. Β_3-adrenoceptor levels and eNOS levels were detected with reverse transcription-polymerase chain reaction ( RT-PCR) and immunohistochemistry. Results LVEDD and LVESD were significantly decreased in the group HTEA compared with group CHF ( P < 0. 01 ) , while LVEF% and LVFS% were significantly increased ( P < 0. 01 ). The ratios HW/BW and LVW/BW were significantly increase in the group CHF compared with the group S(P <0. 01), but they were limited in the group HTEA (P<0. 01). Hypertrophy and edema, degeneration and necrosis of myocytes can be seen in rats with CHF, as well as muscle fibers disruption and collagen fiber increase, while the pathological morphous were attenuated in HTEA rats. Β_3AR and eNOS mRNA levels were significantly decreasedinthegroupTHEA compared with the group CHF. Conclusions These results indicate that HTEA could ameliorate ventricular remodeling and cardiac function in rate with heart failure induced by myocardial infarction. The mechanism could involve decreases of β_3AR expression in rats of heart failure.