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作 者:邓义军[1] 伍卫[1] 方昶[1] 黄至斌[1] 聂如琼[1]
机构地区:[1]中山大学附属第二医院心内科,广东广州510120
出 处:《中国心脏起搏与心电生理杂志》2009年第3期244-246,共3页Chinese Journal of Cardiac Pacing and Electrophysiology
基 金:广东省卫生厅基金资助项目(No.A2007184)
摘 要:目的观察β3-肾上腺素能受体(AR)兴奋对实验性心力衰竭(简称心衰)大鼠心室肌细胞内L-型Ca2+通道(ICa-L)的影响。方法雄性成年Wistar大鼠随机分为心衰组及对照组。通过结扎大鼠冠状动脉前降支制作大鼠实验性心衰模型,经典酶分离法分离心肌细胞,膜片钳技术观察β3-AR激动剂BRL-37344对心室肌细胞ICa-L的影响。结果与对照组比较,心衰心室肌细胞的ICa-L电流明显降低(P<0.05);当膜电位在-20,-10,0,10mV时,BRL37344(1mol/L)降低对照组细胞ICa-L的幅度分别为41.8%、20.0%、15.1%、11.3%(P<0.05);BRL37344(1mol/L)降低心衰组心肌细胞ICa-L的幅度分别为63.0%、40.4%、67.6%、62.8%(P<0.05);同等剂量的BRL37344(1mol/L)降低心衰心室肌ICa-L的幅度大于对照心室肌ICa-L的幅度(P<0.05)。结论β3-AR激动剂可以下调大鼠心室肌细胞内ICa-L,在心衰大鼠心肌ICa-L下调幅度更明显。Objective To observe the effect of β3-Adrenoceptor(AR) on myocytic L-type Ca^2+ channel( ICa-L )in rats with experimental heart failure. Methods Rats were randomized into heart failure group and control group. The experimental heart failure model was built up by ligation of anterior descending coronary artery of rats, and myocytes were isolated with classical enzyme isolation method. The change of ICa-L was determined by patch clamp technique with stimulation of BRL37344 ( β3-AR selective antagonist, 1 mol/L). Results ICa-L was lower in heart failure group than that in control group(P 〈0.05). BRL37344 obvoiously decreased the amplitude of myoctytic ICa-L in control group or heart failure group respectively by 41.8% , 20.0% , 15.1% , 11.3% and 63.0% , 40.4% , 67.6% , 62.8% when membrane potentials was -20, - 10, 0 and 10 mV (P 〈0.05) ; The extent of decrease of ICa-L by BRL37344 was higher in heart failure group than that in control group( P 〈 0.05 ). Conclusion The myoeytic ICa-L, could be downregulated by stimulation of β3-AR and the extent of downregulation in heart failure rats was more than that in rats without heart failure .
关 键 词:电生理学 Β3-肾上腺素能受体 心力衰竭 L-型Ca2+电流
分 类 号:R331.38[医药卫生—人体生理学] R541.61[医药卫生—基础医学]
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