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应用全细胞膜片钳技术研究了皿小板活化因子(platelet activating factor,PAF)对豚鼠心室肌细胞动作电位和钾电流的影响。结果发现,当电极内液ATP浓度为5mmol/L(模拟正常条件)时,1μmol/L PAF使APD_(90)由对照的225.8±23.3ms延长至352.8±29.8ms(n=5,P<0.05);使I_K尾电流在指令电压+30mV由对照的173.5±16.7pA降至152.1±11.5pA(P<0.05,n=4);使I_(K1)在指令电压为-120mV时由对照组的-6.1±1.3nA降至-5.6±1.1nA(P<0.05,n=5);但PAF在生理膜电位范围(-90mV～+20mV)对I_(K1)没有影啊。当电极内液ATP浓度为0mmol/L时,I_(K-ATP)开放(模拟缺血条件),1μmol/L PAF却显著缩短APD_(90),由对照的153±24.6ms缩短至88.2±19.4ms(n=5,P<0.01)。而用1μmol/L格列本脲(I_(K-ATP)的特异阻断剂)预处理后,恢复了PAF可显著延长动作电位时程的作用。结果提示,PAF可能扩大缺血心肌和正常心肌细胞动作电位时程的不均一性,是缺血/再灌注性心律失常发生的重要原因
The effect of platelet activating factor (PAF) on the action potentials and potassium currents of guinea pig ventricular myocytes was investigated by whole-cell patch clamp technique. The results showed that 1μmol / L PAF prolonged APD_ (90) from 225.8 ± 23.3ms to 352.8 ± 29.8ms (n = 5, P <0.05) when the concentration of ATP in electrode was 5mmol / L ). The I_K tail current was reduced from 173.5 ± 16.7pA of the control to 152.1 ± 11.5pA at the command voltage of + 30mV (P <0.05, n = 4) -6.1 ± 1.3nA to -5.6 ± 1.1nA (P <0.05, n = 5). However, PAF had no effect on I_ (K1) in the physiological membrane potential range (-90mV ~ + 20mV) When the concentration of ATP in the electrode was 0mmol / L, I_ (K-ATP) was open (simulated ischemia condition) and 1μmol / L PAF significantly shortened APD_ (90), shortening from 153 ± 24.6ms to 88.2 ± 19.4 ms (n = 5, P <0.01). However, the pretreatment with 1 μmol / L glibenclamide (I-K-ATP) specific blocker restored the effect of PAF on the prolongation of action potential duration. The results suggest that PAF may increase the heterogeneity of the action potential duration of ischemic myocardium and normal cardiomyocyte and is an important reason for the occurrence of ischemia / reperfusion arrhythmia