乳酸酸中毒对兔窦房结优势起搏细胞动作电位的影响

Effects of Lactic Acidosis on the Action Potentials of Rabbit Sinoatrial Node Pacemaker Cells

目的:观察乳酸酸中毒对兔窦房结优势起搏细胞自律性、传导性等电生理的影响。方法:应用玻璃微电极技术,在不缺氧的条件下,观察了17只兔离体窦房结优势起搏细胞在5 mmol/L、10 mmol/L和15 mmol/L3种浓度的乳酸酸中毒条件下动作电位的变化。结果:随着乳酸浓度的增加,动作电位参数发生进行性变化,至15 mmol/L第30 min时,4相自动除极速率及0相除极速率分别降低了48％及38％(均P<0.05),窦房结优势起搏细胞自主起搏周期长度延长了53％(P<0.05),复极90％、50％、30％的动作电位时程分别延长了25％、39％及41％(均P<0.05)。结论:乳酸酸中毒可降低窦房结优势起搏细胞自律性,延缓其传导性,并使动作电位时程延长。

Objective: To evaluate the effects of lactic acidosis on the action potentials of rabbit sinoatrial node pacemaker cells. Methods: The glass microelectrod technique was used to determine the effects of lactic acidosis on the action potentials of sinoatrial node pacemaker cells in 17 rabbit under no hypoxia. Results: V4 and V0 decreased from (69.9± 22.3)mV/s to (36.5±17.0)mV/s, and (0.81±0.31) V/s to (0.50± 0.16) V/s respectively (P<0.05). CLp, APD90, APD50 and APD30 increased from(343.6± 66.4)ms to(526.4±165.2)ms,(139.0±6.5)msto (173.5±35.5)ms, (86.1± 9.6) ms, to(119.3±30.9)ms, and (63.4±8.0)ms to (89.4 ± 3l.6)ms, respectively (P<0.05).Conclusion: Lactic acidosis can reduce V4 and V0, lengthen CLp and APD, decrease automaticity of sinoatrial node pacemaker cells, and slow its conductivity.