【摘要】 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APD₉₀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APD₉₀,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更多还原

【Abstract】 This study was designed to investigate the effects of platelet activating factor （PAF） on the action potential and potassiumcurrents in guinea-pig ventricular myocytes. Whole cell patch clamp techniques were used. With 5 mmol/L ATP in the pipette electrode（mimic normal condition）, 1 μmol/L PAF increased APD₉₀, from 225.8±23.3 to 352.8±29.8 ms （n=5, P<0.05）, decreased I_K1 and I_K tailcurrents from -6. 1±1.3 to -5.6±1.1 nA （n=5, P<0.05） at -120 mV and from 173.5±6.7 to 152.1±11.5 pA （P<0.05, n=4） at+30mV,respectively. But PAF had no effect on I_K1 at potentials within the normal range of membrane potentials （between -90 mV and+20mV）.In the contrary, without ATP in the pipette electrode by which I_K·ATP was activated （mimic ischemic condition）, 1 μmol/L PAF shortenedAPD₉₀ from 153±24.6 to 88.2±19.4 ms （n=5, P<0.01）. Incubation of myocytes with 1 μmol/L glibenclamide, a blocker of I_K·ATP couldrestore prolongation of APD induced by PAF. In conclusion, in guinea-pig ventricular myocytes, with 5 mmol/L ATP in the pipette PAFcould prolong APD partly due to the inhibition of I_K; while with 0 mmol/L ATP in the pipette, PAF could induce an activation of I_K·ATP,hence a decrease in APD. It is suggested that PAF may amplify the heterogeneity between ischemic and normal cardiac myocytes duringischemia/reperfusion, which may play a vital role in the pathogenesis of the arrhythmias induced by ischemia/reperfusion.更多还原