植物雌激素α-ZAL和17βE_2对大鼠单个心室肌细胞缩舒功能和胞内钙瞬时变化的影响

Effects of α-ZAL and 17βE_2 on Cardiac Contractile and Diastolic and Intracellular Ca^(2+) Response in Ventricular Myocytes

目的:比较植物雌激素α-ZAL和17βE2对大鼠心肌细胞缩舒和胞内钙瞬变的影响。方法:从成年雌性大鼠心脏分离单个心肌细胞,应用美国Ionoptix视频跟踪计算机图像分析系统在0.5Hz的电刺激下测定离体单个心肌细胞的收缩参数,其中包括最大收缩幅度(PS)、最大收缩幅度时间(TPS)、90%舒张幅度时间(TR90)和最大收缩速率(+dL/dttmax)及最大舒张速率(-dL/dttmax);同时用Fura2/AM钙荧光指示剂测定胞内钙浓度的变化。结果:10-9~10-5mol/L17βE2能使PS产生浓度依赖性的增加,最大增加35%,高浓度的17βE2对TPS有显著影响(P<0.05),能够使ΔFFI最大增加25%;而10-9~10-5mol/Lα-ZAL无论是心肌细胞缩舒功能还是胞内钙含量均无明显变化。且α-ZAL和17βE2对心室肌细胞静息状态下胞内钙浓度和胞内钙的荧光衰减率均无显著影响。结论:α-ZAL对心室肌细胞的作用与17βE2有很大不同,17βE2对心肌细胞缩舒有直接刺激作用,增强心肌收缩可能是通过胞内钙释放与胞外钙内流所介导;而α-ZAL无这种作用,它可能是通过抑制胞外钙内流和其抗氧化反应达到保护心室肌细胞的作用。

Objective: To compare effects of 17βE_ 2 and phytoestrogen α-ZAL on cardiac mechanical function and intracellular Ca~ 2+ transients in ventricular myocytes.Method: Isolated ventricular myocytes from adult female rats were stimulated to contract at 0.5 Hz. Contractile properties were evaluated using an IonOptixMyoCam system including peak shortening (PS) ,time-to-PS (TPS), time-to-90%(TR_ 90 ) and maximal velocity of shorteningrelengthening ( dLdt). Intracellular Ca~ 2+ properties were evaluated as fura-2 fluorescent intensity change (ΔFFI) and intracellular Ca~ 2+ decay rate. Results: 17βE_ 2 (10~ -9 – 10~ -5 M) elicited a concentration-dependent increase in PS and ΔFFI, with maximal augmentation of ~35% and ~25%, respectively. High concentrations of 17βE_ 2 prolonged TPS although ± dLdt, TR90, resting intracellular Ca~ 2+ level and intracellular Ca~ 2+ decay were unaffected by 17βE_ 2 .None of the mechanical or intracellular Ca~ 2+ indices tested were affected by α-ZAL(10~ -9 – 10~ -5 M).Conclusion: Our results revealed 17βE_ 2 and α-ZAL are made a different in ventricular myocytes ,a direct cardiac stimulatory action from 17βE_ 2 may be induced by intracellular Ca~ 2+ release and extracellular Ca~ 2+ influx;_ but not from α-ZAL on ventricular contraction, its protect effect on ventricular myocytes may be medicated through antioxidation and inhibited extracellular Ca^(2+)influx.