海南医学
海南醫學
해남의학
Hainan Medical Journal
2015年
18期
2668-2670
,共3页
右美托咪定%预处理%缺血再灌注损伤
右美託咪定%預處理%缺血再灌註損傷
우미탁미정%예처리%결혈재관주손상
Dexmedetomidine%Preconditioning%Ischemia reperfusion injury
目的：观察右美托咪定预处理对心肌缺血再灌注损伤的保护作用及心肌细胞钙循环调控蛋白兰尼碱受体(RyR2)和肌浆网钙泵(SERCA2a)的影响。方法45只大鼠随机分为3组，假手术组(Sham组)，缺血再灌注组(I/R组)，右美托咪定预处理组(DEXM组)。DEXM组在缺血前2 h经腹腔注射右美托咪定100μg/kg。监测各组大鼠缺血30 min及再灌注120 min的血流动力学参数评估心功能，以伊文氏蓝-红四氮唑(TTC)染色法测定心肌梗死面积，以实时定量PCR法检测心肌组织RyR2和SERCA2a的mRNA表达水平。结果 I/R组心肌梗死面积(41.5±2.9)%，DEXM组心肌梗死面积(30.8±3.1)%，DEXM组梗死面积明显低于I/R组(P<0.05)。与Sham组及缺血前比较，I/R组和DEXM组缺血30 min及再灌注120 min时，HR、LVDP、±dP/dt均显著降低(P<0.05)， LVEDP显著升高(P<0.05)。I/R组和DEXM组相比，DEXM相LVDP、±dP/dt均高于I/R组(P<0.05)，LVEDP低于I/R组(P<0.05)。I/R组和DEXM组心肌组织中RyR2和SERCA2a的mRNA水平均较Sham组降低(P<0.05)，但DEXM组RyR2和SERCA2a的mRNA水平高于I/R组。结论缺血再灌注前给予右美托咪定预处理可减小心肌梗死面积，促进心肌细胞钙循环，改善心功能，发挥心肌保护作用。
目的：觀察右美託咪定預處理對心肌缺血再灌註損傷的保護作用及心肌細胞鈣循環調控蛋白蘭尼堿受體(RyR2)和肌漿網鈣泵(SERCA2a)的影響。方法45隻大鼠隨機分為3組，假手術組(Sham組)，缺血再灌註組(I/R組)，右美託咪定預處理組(DEXM組)。DEXM組在缺血前2 h經腹腔註射右美託咪定100μg/kg。鑑測各組大鼠缺血30 min及再灌註120 min的血流動力學參數評估心功能，以伊文氏藍-紅四氮唑(TTC)染色法測定心肌梗死麵積，以實時定量PCR法檢測心肌組織RyR2和SERCA2a的mRNA錶達水平。結果 I/R組心肌梗死麵積(41.5±2.9)%，DEXM組心肌梗死麵積(30.8±3.1)%，DEXM組梗死麵積明顯低于I/R組(P<0.05)。與Sham組及缺血前比較，I/R組和DEXM組缺血30 min及再灌註120 min時，HR、LVDP、±dP/dt均顯著降低(P<0.05)， LVEDP顯著升高(P<0.05)。I/R組和DEXM組相比，DEXM相LVDP、±dP/dt均高于I/R組(P<0.05)，LVEDP低于I/R組(P<0.05)。I/R組和DEXM組心肌組織中RyR2和SERCA2a的mRNA水平均較Sham組降低(P<0.05)，但DEXM組RyR2和SERCA2a的mRNA水平高于I/R組。結論缺血再灌註前給予右美託咪定預處理可減小心肌梗死麵積，促進心肌細胞鈣循環，改善心功能，髮揮心肌保護作用。
목적：관찰우미탁미정예처리대심기결혈재관주손상적보호작용급심기세포개순배조공단백란니감수체(RyR2)화기장망개빙(SERCA2a)적영향。방법45지대서수궤분위3조，가수술조(Sham조)，결혈재관주조(I/R조)，우미탁미정예처리조(DEXM조)。DEXM조재결혈전2 h경복강주사우미탁미정100μg/kg。감측각조대서결혈30 min급재관주120 min적혈류동역학삼수평고심공능，이이문씨람-홍사담서(TTC)염색법측정심기경사면적，이실시정량PCR법검측심기조직RyR2화SERCA2a적mRNA표체수평。결과 I/R조심기경사면적(41.5±2.9)%，DEXM조심기경사면적(30.8±3.1)%，DEXM조경사면적명현저우I/R조(P<0.05)。여Sham조급결혈전비교，I/R조화DEXM조결혈30 min급재관주120 min시，HR、LVDP、±dP/dt균현저강저(P<0.05)， LVEDP현저승고(P<0.05)。I/R조화DEXM조상비，DEXM상LVDP、±dP/dt균고우I/R조(P<0.05)，LVEDP저우I/R조(P<0.05)。I/R조화DEXM조심기조직중RyR2화SERCA2a적mRNA수평균교Sham조강저(P<0.05)，단DEXM조RyR2화SERCA2a적mRNA수평고우I/R조。결론결혈재관주전급여우미탁미정예처리가감소심기경사면적，촉진심기세포개순배，개선심공능，발휘심기보호작용。
Objective To investigate the protective effects of dexmedetomidine preconditioning in rats with myocardial ischemia reperfusion injury and the effects of dexmedetomidine on myocardium ryanodine receptor (RyR2) and sarcoplasmic reticIlum Ca2+-ATPase (SERCA2a). Methods Forty-five rats were randomly divided into three groups, sham operation group (Sham group), ischemia-reperfusion group (I/R group) and dexmedetomidine pre-conditioning group (DEXM group). 2 h before left anterior descending coronary artery clamped, DEXM group re-ceived dexmedetomidine 100μg/kg by intraperitoneal injection. The hemodynamic parameters were measured at the time of ischemia 30 min and reperfusion 120 min. The infarct size of myocardial tissues was determined by TTC stain-ing. The mRNA level of RyR2 and SERCA2a were detected by the Real-time PCR. Results The infarct size was (41.5±2.9)%in I/R group, which was significantly higher than (30.8±3.1)%in DEXM group (P<0.05). Compared with the Sham group and the baseline before ischemic, heart rate (HR), left ventricular diastolic pressure (LVDP) and ±dP/dt decreased and the left ventricular end-diastolic pressure (LVEDP) increased in both I/R group and DEXM group at the time of ischemia 30 min and reperfusion 120 min (P<0.05). Compared with the I/R group, LVDP and ±dP/dt were higher, and LVEDP was lower in the DEXM group. Compared with the Sham group, the mRNA level of RyR2 and SERCA2a were smaller in the I/R group and DEXM group, which were higher in DEXM group than in I/R group. Conclusion Dexmedetomidine preconditioning could attenuate myocardial ischemia reperfusion injury in rats via de-creasing infarct size, improving cardiac function and increasing the mRNA level of RyR2 and SERCA2a.
