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引用本文:角灿武,韩圣娜,付润芳,张莉蓉.前列腺素E1预处理对缺血再灌注心肌细胞瞬时外向钾电流和内向整流钾电流的影响[J].中国现代应用药学,2014,31(8):942-946.
JIAO Canwu,HAN Shengna,FU Runfang,ZHANG Lirong.Effects of Pretreatment with Prostaglandin E1 on Transient Outward Potassium Current and Inward Rectifying Potassium Current in Ischemia Reperfusion Myocytes[J].Chin J Mod Appl Pharm(中国现代应用药学),2014,31(8):942-946.
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前列腺素E1预处理对缺血再灌注心肌细胞瞬时外向钾电流和内向整流钾电流的影响
角灿武1, 韩圣娜2, 付润芳2, 张莉蓉2
1.濮阳市人民医院,河南 濮阳457000;2.郑州大学基础医学院药理学教研室,郑州 475001
摘要:
目的 研究前列腺素E1(PGE1)预处理对大鼠缺血再灌注心肌细胞瞬时外向钾电流(Ito)和内向整流钾电流(IK1)的影响。方法 应用Langendorff法制备大鼠离体心肌缺血再灌注模型,酶解法分离单个心室肌细胞,全细胞膜片钳技术记录正常组、缺血再灌注组及不同浓度PGE1预处理组心肌细胞Ito和IK1的变化。结果 在+60 mV刺激电压时,正常大鼠心室肌细胞Ito为(15.54±2.24)pA/pF(n=16),缺血再灌注时Ito减小到(9.99±2.03)pA/pF(n=16),与缺血再灌注组相比, PGE1(14,42,126 μg·L?1)预处理使Ito分别增大到(14.24±1.97)pA/pF(n=17,P<0.05)、(18.41±1.39)pA/pF(n=13,P<0.05)和(21.63±3.2)pA/pF(n=12,P<0.05);Ito半数失活电压(V1/2)由缺血再灌注组的(-18.61±7.81)mV(n=10)分别降低到(-27.95±8.00)mV(n=11,P<0.05)、(-31.34±7.59)mV(n=16,P<0.05)和(-39.50±7.38)mV(n=13,P<0.05)。在-120 mV刺激电压时,PGE1(14,42,126 μg·L?1)预处理使IK1由缺血再灌注组(-11.68±3.82)pA/pF(n=6,P<0.05)分别增大到(-31.89±8.83)pA/pF(n=7,P<0.05)、(-32.36±9.13)pA/pF(n=13,P<0.05)、(-34.70±8.99)pA/pF(n=11,P<0.05)。结论 PGE1预处理能增大大鼠缺血再灌注心室肌细胞Ito及IK1,降低Ito的V1/2
关键词:  前列腺素E1  缺血再灌注  心肌细胞  全细胞膜片钳  瞬时外向钾电流  内向整流钾电流
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Effects of Pretreatment with Prostaglandin E1 on Transient Outward Potassium Current and Inward Rectifying Potassium Current in Ischemia Reperfusion Myocytes
JIAO Canwu1, HAN Shengna2, FU Runfang2, ZHANG Lirong2
1.People’ s Hospital of Puyang, Puyang 457000, China;2.Department of Pharmacology, School of Medicine, Zhengzhou University, Zhengzhou 475001, China
Abstract:
OBJECTIVE To study the effects of prostaglandin E1 (PGE1) pretreatment on transient outward potassium current and inward rectifying potassium current in ischemia/reperfusion cardiomyocytes and explore its possible mechanisms against ischemia/reperfusion injury. METHODS Isolated ischemia/reperfusion model was established according to Langendorff method, enzymatic method was used to isolate single ventricular myocytes, whole-cell patch-clamp was used to record Ito and IK1 in cardiomyocytes of normal group, ischemia/reperfusion group and PGE1 pretreatment group. RESULTS PGE1(14, 42, 126 μg·L?1) pretreatment significantly increased Ito to (14.24±1.97)pA/pF(n=17, P<0.05), (18.41±1.39)pA/pF(n=13, P<0.05) and (21.63±3.2)pA/pF(n=12, P<0.05) respectively from (9.99±2.03)pA/pF(n=16) of ischemia/reperfusion group at the stimulation voltage +60 mV. The half inactivation voltage of Ito were reduced to (-27.95±8.00)mV(n=11, P<0.05), (-31.34±7.59)mV(n=16, P<0.05) and (-39.50±7.38)mV(n=13, P<0.05) respectively from (-18.61±7.81)mV(n=10) of ischemia/ reperfusion group. IK1 were (-11.68±3.82)pA/pF(n=6, P<0.05) in ischemia/reperfusion group at the stimulation voltage -120 mV, but it increased to (-31.89±8.83)pA/pF(n=7, P<0.05), (-32.36±9.13)pA/pF(n=13, P<0.05) and (-34.70±8.99)pA/pF(n=11, P<0.05) respectively following pretreatment with PGE1(14, 42, 126 μg·L?1). CONCLUSION PGE1 pretreatment can increase Ito and IK1 in rat ischemia/reperfusion cardiomyocytes, and decrease the half inactivation voltage of Ito.
Key words:  prostaglandin E1  ischemia/reperfusion  cardiomyocytes  whole-cell patch clamp  transient outward potassium current  inward rectifying potassium current
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