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

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＋60mV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k减小到（9．99±2．03）pA／pF（n=16），与缺血再灌注组相比，PGE1（14，42，126μg·L^-1）预处理使气分别增大到（14．24±1．97）pA／pF（n=17，P＜0．05）、（18．41＋1．39）pA／pF（n=13，P＜O．05）和（21．63±3．2）pA／pF（n=12，P＜0．05）；Uto 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-120mV刺激电压时，PGE1（14，42，126μg-L^-1）预处理使Ik1由缺血再灌注组（-11．68±3．82）pA／pF（n=6，P＜O．05）分别增大到（-31．89±8．83）pA／pF（n=7，P＜0．05）、（-32．36士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It0的V1/2。

Effects of Pretreatment with Prostaglandin E1 on Transient Outward Potassium Current and Inward Rectifying Potassium Current in Ischemia Reperfusion Myocytes

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 /to and IK1 in cardiomyocytes of normal group, ischemia/reperfusion group and PGEl pretreatment group. RESULTS PGEI（14, 42, 126μg·L^-1） pretreatment significantly increased ltotO （14.24±1.97）pA/pF（n=17, P〈0.05）, （18.41±l.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 thestimulation voltage ＋60mV. The half inactivation voltage of /to 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.