【作者】 董江宏；

【导师】 彭鹏；

【作者基本信息】 新疆医科大学 ， 急诊医学， 2010， 硕士

【摘要】 目的:本研究探讨心肺复苏中在自主循环恢复(ROSC)前肾上腺素对大鼠心肌的损伤情况,以及心肌损伤与β1-肾上腺素能受体(β1-AR)的关系及可能机制。方法:SD雄性大鼠50只,随机分为4组:空白对照组(A组、10只)、复苏对照组(B组、10只)、标准剂量肾上腺素组(C组、15只)、大剂量肾上腺素组(D组、15只)。采用大鼠心肺复苏模型,麻醉大鼠、气管切开置管、动静脉插管,除了正常对照组不诱发心脏骤停外,其余组均在呼气末夹闭气管插管,中断通气,致大鼠心跳骤停。大鼠心跳骤停5min后松开夹闭的气管,连接呼吸机辅助呼吸,同时进行快速胸外心脏按压,经尾静脉注射肾上腺素。标准剂量组、大剂量组在2.5±0.5min出现自主心律、脉搏波、平均动脉压(MAP)≥60mmHg,停止复苏观察15秒后剖胸取心脏留标本。复苏对照组不注射肾上腺素,在心外按压2.5min后直接剖胸取心脏留标本。检测各组心肌组织,用硫代巴比妥酸比色法检测大鼠心肌组织丙二醛(MDA)浓度;用黄嘌呤氧化法检测大鼠心肌组织超氧化物歧化酶(SOD)活力;用定磷法检测心肌组织Na+K+-ATP酶的活力;应用双抗体夹心酶标免疫分析法测定大鼠心肌组织匀浆并计算环磷腺苷(cAMP)浓度;记录心外按压时平均动脉压;电镜观察心肌细胞超微结构变化。结果:1)检测心肌组织MDA发现,未用肾上腺素的复苏对照组比标准剂量组、大剂量组心肌MDA浓度低(P<0.01),标准剂量组心肌MDA浓度比大剂量组低(P<0.05);2)检测心肌组织Na+K+-ATP酶和SOD活力发现,复苏对照组比标准剂量组、大剂量组心肌Na+K+-ATP酶和SOD活力高(P<0.01),标准剂量组心肌ATP酶和SOD活力比大剂量组高(P<0.01);3)复苏对照组心肌cAMP含量比标准剂量组、大剂量组低(P<0.01),标准剂量组与大剂量组心肌cAMP含量无统计学差异(P>0.05);4)心外按压时标准剂量组平均动脉压比大剂量组低(P<0.01)。大剂量组心肌纤维变细,各带线结构显示不清,部分肌丝溶解,线粒体水肿、空泡化,线粒体峭排列紊乱,细胞浆内糖原颗粒减少等,而在标准剂量组亦发现上述超微结构变化,但是比大剂量组损伤程度轻。结论:在心肺复苏中,比较对照组,大剂量和标准剂量肾上腺素组在自主循环恢复前就已经加重了心肌组织的损伤,大剂量组心肌损伤更为明显;在自主循环恢复前加重心肌损伤可能不是心肌β1-AR激活引起,其可能的损伤机制需要进一步的实验研究。更多还原

【Abstract】 Objective: After cardiopulmonary resuscitation, cardiac insufficiency is important reason that death rate of patient is high at acute stage. To investigate epirenamine’s myocardial damage condition before ROSC’rat, during CPR. To investigate relationehip and possible mechanism between myocardial damage andβ1-AR. Methods: Fifty SD male were randomly divided into groups 4: blank group (A, n=10); resuscitation control group (B, n=10); standard-dose epinephrine group (C, n=15); high-dose epinephrine group (D, n=15) .To apply rat CPR’model, to anesthetize experimental rat, incision of trachea and to put arterial and venous cannual. except blank group, the rest group will occlude trachea cannula at end expiration, to result rat’s cardiac arrest. After 5 min of rat’s cardiac arrest, trachea cannula would be unclamped to connect breathing machine and assist respiration, meanwhile we would carry out closed cardiac massage and inject epinephrine through caudal vein. Groups C and D will stop CPR and observe for 15 second to remain heart’s sample after appearing independent cardiac rhythm. Pulse wave arterial blood pressure (MAP)≥60mmhg, group B don’t inject epinephrine and directly remain heart’s sample after 30 secend of closed cardiac massage. This sample would be detected for vigor of ATPase, SOD and concentration of MDA, cAMP, then to take statistical analysis. Heart’s sample would be observed ultramicrostructure of cardic muscle cell through electron microscope. Results: Concetration of cardiac muscle’MDA in groups A?B is lower than groups C, D (P<0.01). Concetration of cardiac muscle’MDA in group C is lower than groups D (P<0.05).Vigors of cardiac muscle’ATPase, SOD in groups A, B is higher than groups C, D (P<0.01), and group C is higher than group D (P<0.01). There was no significant difference in cardiac muscle’cAMP concentration between group C and group D (P>0.05). Transmission electron microscopy showed the myocardial cell damage performance in rats after CPR. Nuclear deformation, marginated chromatin, the nuclear membrane rupture, pyknosis, mitochondrial swelling, ridge fracture or even disappear.There was significant difference between group C and group D in observing ultramicrostructure of cardiac muscle cell. Conclusion: During CPR, high-dose epinep- hrine has increased myocardial damage before ROSC compare with standard-dose epinephrine, but high-dose epinephrine has increased myocardial damage which might be not effect ofβ1-AR’increased excitability.更多还原