Abstract:
OBJECTIVE To study the effects of prostaglandin E
1 (PGE
1) 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 I
to and I
K1 in cardiomyocytes of normal group, ischemia/reperfusion group and PGE
1 pretreatment group. RESULTS PGE
1(14, 42, 126 μg·L
?1) pretreatment significantly increased I
to 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 I
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. I
K1 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 PGE
1(14, 42, 126 μg·L
?1). CONCLUSION PGE1 pretreatment can increase I
to and I
K1 in rat ischemia/reperfusion cardiomyocytes, and decrease the half inactivation voltage of I
to.