摘要
目的 :观察在缺血条件下 ,溶血磷脂酰胆碱 (LPC)对心肌起搏离子流 (If)的影响以及能否被异丙肾上腺素(ISO)逆转。方法 :采用双微电极电压钳制术 ,在各钳制电位测定并比较缺血心肌加入LPC和LPC加ISO的起搏离子流 (If)幅值。结果 :缺血降低If 幅值 ,在模拟缺血液中加入LPC 2× 10 -5mol/L ,If 幅值在Ec - 80～ - 12 0mV水平进一步显著降低 (n =5 ,P <0 .0 5 ) ,加重了缺血对If 离子流的抑制作用。在模拟缺血液中同时加入LPC 2×10 -5mol/L和ISO 1× 10 -6mol/L ,If 幅值在Ec - 90～ - 12 0mV水平比模拟缺血时有显著增加 (n =8,P <0 .0 5 ) ,但未能达到缺血前基础水平。结论 :急性心肌缺血时 ,毒性代谢产物LPC加重起搏离子流的受抑程度 ,即使局部儿茶酚胺大量释放和积聚 ,也不能完全逆转上述抑制效应。
Aim: To observe the effect of LPC on the pacemaker current I f in ischemic myocardium and if the effect could be reversed by ISO. Methods: By using two microelectrode voltage clamp technique to measure and compare the amplitude of I f of ischemic myocardium in the presence of LPC and LPC add ISO. Results:Ischemia decreased the amplitude of I f at all membrane potential levels. Adding LPC 2×10 -5 mol/L to the ischemia-like solution,the amplitude of I f decreased further(n=5,P<0.05),it means that LPC aggravated the inhibitory effect of 'ischemia' on the pacemaker activity. Adding LPC 2×10 -5 mol/L and ISO 1×10 -6 mol/L together to the ischemia-like solution,the amplitude of I f increased significantly at membrane potential -90 mV to -120 mV (n=8,P<0.05) compared with ischemia condition, but still did not reach the levels before ischemia. Conclusion: In acute myocardial ischemia condition,toxic metabolite LPC accentuated its inhibitory effect on pacemaker current I f,a local release and accumulation of catecholamine could not completely reverse their inhibitory effect.
出处
《中国应用生理学杂志》
CAS
CSCD
北大核心
2004年第1期1-5,共5页
Chinese Journal of Applied Physiology
基金
卫生部资助课题 (94 1 3 13 )
