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作 者:郭彩霞[1] 张立克[2] 王红霞[2] 芦玲巧[2] 杜凤和[1]
机构地区:[1]首都医科大学附属北京天坛医院心内科,北京100050 [2]首都医科大学病理生理教研室,北京100054
出 处:《中国急救医学》2010年第3期234-237,共4页Chinese Journal of Critical Care Medicine
基 金:国家自然科学基金资助项目(No.30740054)
摘 要:目的探讨急性脑损伤(acute brain injury,ABI)致心肌损害的内源性去甲肾上腺素(noradrenaline,NE)和β1肾上腺素受体(adrenalin β1 receptor,β1—AR)变化,为了解ABI致心肌损害的发生机制提供理论依据。方法采用动物模型观察肌酸磷酸激酶同工酶(MB isoenzyme of creatine kinase,CK—MB)含量判断心肌损害与否及损伤程度,采用高效液相色谱-电化学检测(( high performance liquid chromatogramphy - electrical conductivity detector, HPLC - ECD)测定血浆及心肌组织NE水平,观察1、6、24和48h时间点的变化。采用反转录多聚酶链反应(reverse tran-scriptase polymerase chain reaction, RT- PCR)和实时定量反转录多聚酶链反应(real-time RT-PCR,rt-RT—PCR)测定β1-ARmRNA表达。实验分为正常组、假手术组、ABI组和β1肾上腺素受体阻断剂(adrenalin β1 receptor blocker, β1 - ARB )组。结果ABI致心肌损害表现为CK—MB含量显著增加(P〈0.05),脑损伤后24h心肌损害最严重。血浆和心肌组织NE水平显著升高(P〈0.05),血浆NE水平与CK—MB含量呈正相关(P〈0.05)。ABI及预先应用β1-AR阻断剂后心肌组织β1-ARmRNA表达与对照组相比差异元统计学意义。结论ABI可导致心肌损害的发生,可增加内源性NE,NE可能是参与急性脑损伤后心肌损害的机制之一。Objective To discuss changes of endogenetic NE and myocardial β1 - AR in the myocardial damage after acute brain injury(MDABI) for better understanding the mechanism. Methods Acute brain injury(ABI) rat model was induced. CK- MB in serum was measured to indicate the degree of myocardial damage. NE in plasma and myocardium were detected by HPLC - ECD. Changes were observed in4 time point including 1 h, 6 h, 24 h and 48 h after ABI. Expression of β1 - AR mRNA was determined by RT - PCR and real - time RT - PCR. There were four groups in the experiment including normal, sham, ABI and β1 -ARB group. Results CK- MB increased in the MDABI. The most severe myocardial damage happened in 24 hours after ABI. NE in plasma and myocardium increased significantly( P 〈 0. 05 ). Positive correlation was found between NE in plasma and CK- MB(P 〈 0. 05 ). There was no significant difference of myocardial β1 -AR mRNA between ABI group and SHAM group. Same result happened between β1 - ARB group and SHAM group. Conclusion ABI can lead to myocardial damage. The endogenetic NE increased in the ABI, which maybe one of the mechanism of MDABI.
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