大鼠心脏骤停心肺复苏后心功能不全模型的构建

Establishment of cardiac dysfunction model after cardiopulmonary resuscitation in rats with cardiac arrest

目的建立大鼠心脏骤停心肺复苏(CA-CPR)后心功能不全模型。方法采用冰氯化钾停跳联合窒息4 min、人工胸外心脏按压3 min的方法,建立CA-CPR模型。30只雄性SD大鼠分为2组:假手术组(n=15)仅置入相关导管,不行CPR术;CPR组(n=15)置入相关导管,行CPR术。术后连续监测4 h血流动力学:平均动脉压(MBP)、左室内压最大上升速率(dp/dtmax)及左室内压下降速率(-dp/dt)。透射电镜观察大鼠心肌组织超微结构。乳酸-丙酮酸法检测血清乳酸脱氢酶(LDH)活性。ELISA法测血清肌酸激酶同工酶(CK-MB)浓度。结果 CPR组复苏后各时间点MBP、dp/dtmax、-dp/dt均显著低于复苏前(P<0.05)。CPR组MBP、dp/dtmax、-dp/dt在复苏后各时间点显著低于假手术组(P<0.05)。与假手术组相比,CPR组心肌超微结构损伤明显,LDH活性、CK-MB浓度明显增高(P<0.05)。结论本实验成功建立了大鼠心脏骤停心肺复苏复苏后心功能不全模型,此模型稳定可靠,为探讨复苏后心功能不全的保护措施提供了模型基础。

Objective To establish the cardiac dysfunction model after cardiopulmonary resuscitation in rats with cardiac arrest. Methods The CA - CPR model was established by intravenous injection potassium chloride （4 ℃ ） combined with asphyxiation for 4 min and then followed by artificial chest compression for 3 min. Thirty male SD rats were divided into two groups ： sham - operated group （with relevant catheter only, no CPR, n = 15 ） and CPR group （with inserted related catheters and being performed CPR, n = 15 ）. Mean arterial pressure （MBP）, the maximal derivatives of left ventricular pressure （dp/dtmax）, and the maximal rate of pressure de- cline （-dp/dt） were monitored continuously for 4hrs after resuscitation （catheterization）. The ultrastructure of rat myocardial tissue was observed by transmission electron microscope. Serum samples were taken 4hrs after resuscitation （catheterization）, and lactate de- hydrogenase （LDH） activity was measured by lactate- pyruvate method. Serum creatine kinase isoenzyme （CK- MB）concentration was measured by ELISA. Results In CPR group, The MBP, dp/dtmax, and - dp/dt were significantly lower at different time points af- ter resuscitation than those before CPR （P 〈 0.05 ） ; MBP, dp/dtmax, - dp/dt in CPR group were significantly lower than those in sham operation group at each time point after resuscitation （ P 〈 0.05 ） ; Compared with sham - operated group, uhrastructural damage in myocardial was significant in CPR group ; Compared with sham - operated group, LDH activity and CK - MB concentration in CPR group were significantly higher （ P 〈 0.05 ）. Conclusion The model of cardiac dysfunction after cardiopulmonary resuscitation （ CA - CPR） in rats are successfully established, and the model is stable and reliable, and to provide a good model basis for exploring protection meas- ures of post - resuscitation cardiac dysfunction.