Inhibition of SK channels protects against ventricular fibrillation (VF)in anesthetized rats with ac

• 作 者: GuiLe[1]XiaotongQin[1]MinPan[1]ZixiCheng[2]JianhuaZhu[1]Qing-HuiChen[3]
• 机 构: Department of Cardiology,Affiliated Hospital of Nantong Univ,Jiangsu,China
• 出 处: International Conference for Physiological Sciences 2012(201
• 发表日期: 2012年期

　　In vitro study has shown that activation of SK channels in the ventricular myocytes is responsible for the VF in failing ventricle.This study determined the role of SK channels in regulating VF in AMI rats.AMI was induced by coronary artery ligation and ventricular programmed stimulation was used to evaluate ventricular vulnerable period (VVP), VF threshold (VFT) and ventricular effective refractory period (VERP).In AMI,VVP was prolonged and VERP was shortened (P<0.05).Pre-treatment with the SK channel blocker UCL1684 significantly shortened VVP and prolonged VERP No effects were observed in sham-operated rats.VFT was reduced in the AMI, and UCL1684 increased VFT (P<0.05), but was without effect in sham-operated rats.Monophasic action potential duration (MAPD90) recorded from the left ventricular epicardium was shortened in AMI (P<0.05), and UCL1684 significantly prolonged the MAPD90, but was without effect in sham-operated rats.We conclude that activation of SK channels may underlie the mechanisms of VF.Inhibition of SK channels reduced shorting of MAPD90, which may be responsible for the inhibitory effect on VF in AMI.