Hu Y M, Zhang Z, Gao R B, Xu Y Q
Department of Physiology, Shanghai Second Medical University.
Sheng Li Xue Bao. 1997 Oct;49(5):513-20.
By using two microelectrode voltage clamp technique, the effects of "ischemia" and lysophosphatidylcholine (LPC), a main toxic metabolite in acute ischemic myocardium, on pacemaker current I(f) were examined in sheep cardiac Purkinje fibers. After perfusion with ischemia-like solution for 15, 30 and 60 min, the amplitude of I(f) current was decreased at all membrane potential levels between -60 mV (-) -120 mV (n = 5, P < 0.05), both the activation time and half activation time reaching a steady state value were prolongated (n = 5, P < 0.05), with a result of shifting activation curve of I(f) to a more hyperpolarizing level. In normal Tyrode solution, the amplitudes of I(f) at all measured potential levels were decreased significantly by LPC 2 x 10(-5) mol/L (n = 10, P < 0.05); the steady-state activation curve of I(f) was shifted to a more hyperpolarizing level but the activation time and half activation time to a steady-state value were not changed. When 2 x 10(-5) mol/L LPC was added to the solution after 30 min "ischemia", the amplitude of I(f) decreased significantly at all measured membrane potentials and further more for another 15 min (n = 10, P < 0.05). This suggests that ischemic metabolite LPC may have an inhibitory effect on the normal pacemaker activity of ventricle. Ischemic-like condition could aggravate the suppression of LPC without inducing abnormal strengthening of normal automatic rhythmic activity that might lead to ventricular tachyarrhythmia.
采用双微电极电压钳技术,在绵羊心脏浦肯野纤维中研究了“缺血”及急性缺血心肌中的主要毒性代谢产物溶血磷脂酰胆碱(LPC)对起搏电流I(f)的影响。用类缺血溶液灌注15、30和60分钟后,在-60 mV至-120 mV之间的所有膜电位水平,I(f)电流幅度均降低(n = 5,P < 0.05),激活时间和半激活时间达到稳态值均延长(n = 5,P < 0.05),结果是I(f)的激活曲线向更超极化水平移动。在正常台氏液中,2×10⁻⁵ mol/L的LPC使所有测量电位水平的I(f)幅度显著降低(n = 10,P < 0.05);I(f)的稳态激活曲线向更超极化水平移动,但激活时间和达到稳态值的半激活时间未改变。在“缺血”30分钟后向溶液中加入2×10⁻⁵ mol/L的LPC,在所有测量的膜电位下,I(f)幅度均显著降低,并在接下来的15分钟内进一步降低(n = 10,P < 0.05)。这表明缺血代谢产物LPC可能对心室的正常起搏活动有抑制作用。类缺血状态可加重LPC的抑制作用,而不会诱导可能导致室性快速心律失常的正常自动节律活动异常增强。