氧自由基致豚鼠心室肌细胞跨膜电位变化的离子电流基础

IONIC CURRENT BASIS FOR OXYGEN RADICAL-INDUCED CHANGE OF TRANSMEMBRANE POTENTIAL IN GUINEA PIG VENTRICULAR MYOCYTES

目的 :旨在揭示氧自由基参与缺血 /再灌注性心律失常发生的离子电流基础。方法 :采用膜片钳全细胞式记录技术 ,观察H2 O2 ( 1mmol/L)对豚鼠心室肌细胞跨膜电位和相关离子电流的影响。结果 :H2 O2 使豚鼠心肌单细胞的静息电位 (RP)降低 ,动作电位时程 (APD)显著缩短 ,对动作电位幅度 (APA)和超射 (OS)及钠电流的峰值 (INa)均无明显影响 ;明显抑制内向整流钾电流 (IK1) ,尤其在超极化时 ;增强延迟外向钾电流 (IK) ,尤其快组分 (IKr)增加显著 ,而慢组分 (IKs)增加不十分显著 ;抑制或取消L 型钙电流 (ICa)。结论 :活性氧所致心室细胞跨膜电位的变化具有明显的离子电流基础 。

Aim: To reveal ionic current basis for oxygen radical induced ischemic reperfusion arrhythmias. Method: We investigated the effect of H 2O 2(1 mmol/L) on the transmembrane potential and ionic currents in guinea pig ventricular myocytes using whole cell recording patch clamp method. Results: H 2O 2 reduced resting potential (RP) of ventricular myocytes in guinea pig, and shortened action potential duration (APD) significantly; action potential amplitude (APA), overshed (OS) and surrium current (I Na ) were unaffected markedly; suppressed the inward rectifier K+ current (I KI ) significantly, especially at hyperpolarization; enhanced the delayed outward K+ cuuent (I K), particularly the rapid component of the delayed rectifier K+ current (I Kr ); suppressed or abolished Ltype of calcium current (I Ca ). Conclusion: The change of transmembrane potential in the ventricular myocytes induced by active oxygen have an evident ionic current basis. This is the probable mechanism for oxygen radical induced arrhythmias.