中华急诊医学杂志
中華急診醫學雜誌
중화급진의학잡지
CHINESE JOURNAL OF EMERGENCY MEDICINE
2011年
7期
698-702
,共5页
晏平%陈寿权%李章平%章杰%薛继可%王万铁%黄唯佳%程俊彦%李惠萍
晏平%陳壽權%李章平%章傑%薛繼可%王萬鐵%黃唯佳%程俊彥%李惠萍
안평%진수권%리장평%장걸%설계가%왕만철%황유가%정준언%리혜평
心搏骤停%心肺复苏%心肌损伤%磷酸肌酸%细胞凋亡%Bcl-2%Bax%TUNEL
心搏驟停%心肺複囌%心肌損傷%燐痠肌痠%細胞凋亡%Bcl-2%Bax%TUNEL
심박취정%심폐복소%심기손상%린산기산%세포조망%Bcl-2%Bax%TUNEL
Cardiac arrest%Cardiopulmonary resuscitation%Myocardial injury%Phosphocreatine%Apoptosis%Bcl-2%Bax%TUNEL
目的 通过观察大鼠心肺复苏(CPR)后心肌细胞凋亡及凋亡相关蛋白Bax,Bcl-2的表达及外源性磷酸肌酸(CP)干预的影响,研究大鼠CPR后心肌损伤机制及外源性CP的保护作用.方法 将32只成年雄性SD大鼠随机分为对照组(A组)、常规复苏组(B组)、常规剂量CP组(C组,胸外按压时首次给药CP 0.5g/kg,2 h后再次给药1.0g/kg)、大剂量CP组(D组,胸外按压时首次给药CP 1.0g/kg,2 h后再次给药2.0g/kg).每组动物8只.建立窒息型大鼠心搏骤停(CA)-CPR模型,ROSC后24 h取心肌标本待测.以脱氧核糖核昔酸末端转移酶介导的缺口末端标记法(TUNEL)检测ROSC后24h的心肌细胞凋亡指数(AI);以免疫组化法检测ROSC后24h的心肌细胞Bcl-2,Bax蛋白表达.数据比较采用方差分析.结果 与A组比较,CPR后24h B,C,D各组心肌凋亡指数及Bax,Bcl-2蛋白表达均显著升高(均P＜0.01),Bcl-2/Bax值均明显降低(P＜0.01);与B组比较,C组和D组心肌的凋亡指数及Bax,Bcl-2蛋白表达均明显降低,Bcl-2/Bax值均明显上升(P＜0.01);与C组比较,D组的凋亡指数及Bax,Bcl-2蛋白表达均明显降低,Bcl-2/Bax值明显上升(P＜0.05).结论 外源性磷酸肌酸可明显抑制窒息型大鼠CPR后心肌细胞凋亡,对心肺复苏后心肌损伤具有保护作用,该作用以大剂量时更明显.
目的 通過觀察大鼠心肺複囌(CPR)後心肌細胞凋亡及凋亡相關蛋白Bax,Bcl-2的錶達及外源性燐痠肌痠(CP)榦預的影響,研究大鼠CPR後心肌損傷機製及外源性CP的保護作用.方法 將32隻成年雄性SD大鼠隨機分為對照組(A組)、常規複囌組(B組)、常規劑量CP組(C組,胸外按壓時首次給藥CP 0.5g/kg,2 h後再次給藥1.0g/kg)、大劑量CP組(D組,胸外按壓時首次給藥CP 1.0g/kg,2 h後再次給藥2.0g/kg).每組動物8隻.建立窒息型大鼠心搏驟停(CA)-CPR模型,ROSC後24 h取心肌標本待測.以脫氧覈糖覈昔痠末耑轉移酶介導的缺口末耑標記法(TUNEL)檢測ROSC後24h的心肌細胞凋亡指數(AI);以免疫組化法檢測ROSC後24h的心肌細胞Bcl-2,Bax蛋白錶達.數據比較採用方差分析.結果 與A組比較,CPR後24h B,C,D各組心肌凋亡指數及Bax,Bcl-2蛋白錶達均顯著升高(均P＜0.01),Bcl-2/Bax值均明顯降低(P＜0.01);與B組比較,C組和D組心肌的凋亡指數及Bax,Bcl-2蛋白錶達均明顯降低,Bcl-2/Bax值均明顯上升(P＜0.01);與C組比較,D組的凋亡指數及Bax,Bcl-2蛋白錶達均明顯降低,Bcl-2/Bax值明顯上升(P＜0.05).結論 外源性燐痠肌痠可明顯抑製窒息型大鼠CPR後心肌細胞凋亡,對心肺複囌後心肌損傷具有保護作用,該作用以大劑量時更明顯.
목적 통과관찰대서심폐복소(CPR)후심기세포조망급조망상관단백Bax,Bcl-2적표체급외원성린산기산(CP)간예적영향,연구대서CPR후심기손상궤제급외원성CP적보호작용.방법 장32지성년웅성SD대서수궤분위대조조(A조)、상규복소조(B조)、상규제량CP조(C조,흉외안압시수차급약CP 0.5g/kg,2 h후재차급약1.0g/kg)、대제량CP조(D조,흉외안압시수차급약CP 1.0g/kg,2 h후재차급약2.0g/kg).매조동물8지.건립질식형대서심박취정(CA)-CPR모형,ROSC후24 h취심기표본대측.이탈양핵당핵석산말단전이매개도적결구말단표기법(TUNEL)검측ROSC후24h적심기세포조망지수(AI);이면역조화법검측ROSC후24h적심기세포Bcl-2,Bax단백표체.수거비교채용방차분석.결과 여A조비교,CPR후24h B,C,D각조심기조망지수급Bax,Bcl-2단백표체균현저승고(균P＜0.01),Bcl-2/Bax치균명현강저(P＜0.01);여B조비교,C조화D조심기적조망지수급Bax,Bcl-2단백표체균명현강저,Bcl-2/Bax치균명현상승(P＜0.01);여C조비교,D조적조망지수급Bax,Bcl-2단백표체균명현강저,Bcl-2/Bax치명현상승(P＜0.05).결론 외원성린산기산가명현억제질식형대서CPR후심기세포조망,대심폐복소후심기손상구유보호작용,해작용이대제량시경명현.
Objective To observe the changes of cell apoptosis and levels of Bcl-2 and Bax protein in myocardium after cardiopulmonary resuscitation (CPR) in rats and to study the protective effects of different doses of exogenous phosphocreatine (creatine phosphate, CP) on cell apoptosis. Methods A total of 32 male adult SD rats were randomly divided into 4 groups, namely control group ( group A), CPR group (group B), low dose CP group (group C, phosphocreatine 0. 5 g/kg given at beginning of CPR and 1.0 g/ kg 2 hour after CPR) and high dose CP group ( group D, phosphocreatine 1.0 g/kg at beginning of CPR and 2. 0 g/kg 2 hours after CPR) . Cardiac arrest was induced by asphyxiation and CPR was started 7 min after asphyxiation it groups B, C and D. Myocardium samples were taken 24 hours after CPR for detecting myocardium cell apoptosis by TUNEL method. The levels of Bcl-2 and Bax protein were measured by using immunohistochemistry. Experimental data were processed with variance analysis in SPSS package. Results Compared with group A, myocardium cell apoptosis index (AI), and the levels of Bcl-2 and Bax proteinincreased significantly in groups B, C and D (P ＜0. 01 ), and Bcl-2/Bax ratio decreased significantly (P ＜0. 01 ) . Compared with group B, myocardium cell AI and levels of Bcl-2 and Bax protein decreased significantly in groups C and D ( P ＜ 0. 01 ), and Bcl-2/Bax ratio increased significantly ( P ＜ 0. 01 ) .Compared with group C, myocardium cell AI and levels of Bcl-2 and Bax decreased significantly in group D (P ＜ 0. 05 ), and Bcl-2/Bax ratio increased significantly ( P ＜ 0. 05 ) . Conclusion Exogenous phosphocreatine, especially inlarge dose, could inhibit apoptosis of myocardium cells and alleviate myocardium injury after CPR in rats.
