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作 者:方开云[1] 何祥[1] 史静[2] 高鸿[2] 安裕文[2]
机构地区:[1]贵州省人民医院麻醉科,贵阳市550002 [2]贵阳医学院附属医院麻醉科
出 处:《临床麻醉学杂志》2011年第8期818-819,共2页Journal of Clinical Anesthesiology
摘 要:目的观察丙泊酚对离体家兔心脏电生理和心肌β1肾上腺素受体蛋白表达的影响,探讨其引起心率减慢的原因。方法健康家兔24只,随机均分为三组。开胸后迅速取出心脏,将心脏连接于Laugendorff离体灌注装置,用K-H液进行恒温恒压逆行灌注,平衡15 min后,C组持续灌流正常K-H液;P1、P2组分别灌注含丙泊酚4、12μg/ml的K-H液;35 min后,测定HR、窦房传导时间(SACT)、窦房结功能恢复时间(SNRT)、校正SNRT(CSNRT)、房室传导文氏现象的最低心房起搏频率(WB)和出现2∶1房室传导的最低心房起搏频率(2∶1 B)。测定完毕留取右心房心肌组织用Western Blotting检测心肌β1肾上腺素受体蛋白的表达。结果与C组和P1组比较,P2组HR明显减慢,SACT、SNRT和CSNRT显著延长(P<0.05),WB和2∶1 B频率显著缩短(P<0.05)。三组β1肾上腺素受体蛋白的表达差异无统计学意义。结论丙泊酚可以抑制心脏传导系统功能但不影响心脏β1肾上腺素受体蛋白的表达,其引起的心率减慢可能部分是由于抑制了心脏传导系统功能。Objective To investigate the effects of propofol on cardiac electrophysiology and the expression of cardiac β1-adrenoreceptors in isolated rabbit heart and to explore the mechanisms of propofol-induced bradyarrhythmias. Methods Twenty-four rabbits were equally randomized into three groups( n = 8 ). After completion of dissection and instrumentation according to the Langendorff technique, the hearts were allowed to equilibrate for 15 min before the experimental protocols began. Then the isolated hearts were perfused with oxygenated Krebs-Henseleit (K-H) buffer solution (95% 02 +5 %CO2) in group C(control group), K-H buffer with 4 μg/ml and 12μg/ml propofol in group P1 and group P2 respectively for 35 minutes. Then HR, sinoatrial conduction time (SACT), sinus node recovery time(SNRT), corrected sinus node recovery time (CSNRT), Wenckebach block rate and 2: 1 block rate were measured. The right atrial myocardium was taken to estimate the expression of β1-adrenoreceptor protein by western blotting. Results A high concentration of propofol (group P2 ) caused a significant decrease in HR, wenckebach block rate and 2: 1 block rate, and a significant prolongation of SNRT, corrected SNRT and SACT as compared with group P1 and group C (P〈 0. 05), No statistically difference was observed in the expression level of β1-adrenoreceptor protein among groups. Conclusion Propofol can suppress conduction function of heart without affecting the expression of β1-adrenoreceptor protein, which may explain for clinical observations of propofolcaused severe bradyarrhythmias.
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