氨茶碱对三磷酸腺苷诱发兔窦房结电生理反应的抑制作用

目的　分析氨茶碱对三磷酸腺苷 (ATP)诱发兔窦房结电生理反应的抑制作用。方法　细胞内微电极技术记录兔离体窦房结细胞动作电位。结果　ATP( 0 3～ 3 0mmol/L)单次槽内注入给药 ,浓度依赖性减慢窦房结自发搏动速率 2 2 %～ 4 3% ,降低舒张期除极速率 4 2 9%～ 6 6 7% ,增大动作电位幅值 7 1%～ 9 2 % ,加快最大除极速率 32 0 %～ 75 5 % ,使动作电位复极 5 0 %和 90 %的时程 (APD50 和APD90 )缩短 7 1%～ 11 8%和7 3%～ 9 3%。P1受体阻断剂氨茶碱 ( 0 1mmol/L)显著拮抗ATP的作用 ,P2受体阻断剂反应蓝 2( 0 0 5mmol/L)则不影响ATP的作用。结论　ATP的上述电生理学效应可能通过P1受体介导

Inhibitory effects of aminophylline on the electrophysiological responses to adenosine triphosphate in the rabbit sinoatrial node pacemaker cells

Objective To study the inhibitory effect of aminophylline on the electrophysiological responses to adenosine triphosphate (ATP) in the rabbit sinoatrial node pacemaker cells.Methods Intracellular microelectrode method was used to record the parameters of action potential in the rabbit sinoatrial nodes. Results ATP (0 3～3 mmol/L) decreased the rate of pacemaker firing by 22%～43% and velocity of diastolic depolarization by 42 9%～66 7%, increased the amplitude of action potential(AP) by 7 1%～9 2% and maximal rate of depolarization by 32 0%～75 5%,shortened action poteutial duration (APD 50 ) by 7 1%～11 8% and APD 90 by 7 3%～9 3%,all being concentration dependent.The electrophysiological effects of ATP on pacemaker cells were significantly inhibited by P1 receptor antagonist aminophylline at 0 1 mmol/L,and the effects of ATP were not significantly affected by P2 receptor antagonist reactive blue 2 at 0 05 mmol/L.Conclusion The electrophysiological effects of ATP in the rabbit sinoatria lnode pacemaker cells might be mediated via P1 receptors.