前胡丙素对培养乳鼠心肌细胞自发性收缩及动作电位的影响

EFFECTS OF PRAERUPTORIN C ON SPONTANEOUS CONTRACTION AND ACTION POTENTIAL IN CULTURED MYOCARDIAL CELLS OF NEONATAL RATS

用倒置显微镜闭路电视系统及细胞内标准微电极法，记录培养心肌细胞的自发性收缩及动作电位，结果发现：应用Ｐｒａ－Ｃ５ｍｉｎ后，心肌细胞收缩频率及细胞边缘运动的速度同时下降。Ｐｒａ－Ｃ１０，３０和１００μｍｏｌ·Ｌ－１剂量依赖性的方式抑制心肌细胞的收缩速度，分别抑制２４％，４３％和５０％。ｐｒａ－Ｃ（１０和３０μｍｏｌ·Ｌ－）显示了抑制心肌细胞收缩频率的作用，分别抑制１３％和１９％。Ｎｉｆ３μｍｏｌ．Ｌ－１分别缩短ＡＰＤ５０和ＡＰＤ９０１４％及１７％，但同样浓度的ｖｅｒａｐａｔｍｉｌ则抑制ＡＰＡ２７％，缩短ＡＰＤ５０８％，分别延长ＡＰＤ９０及ＳＣＬ１０％和４３％。Ｐｒａ－Ｃ１０，３０和１００μｍｏｌ·Ｌ－１缩短ＡＰＤ５０７％，１４％和１８％。Ｐｒａ－Ｃ１００μｍｏｌ·Ｌ－１有抑制ＡＰＡ及延长ＳＣＬ的作用。结果提示，Ｐｒａ－Ｃ对心肌细胞收缩及动作电位的作用可能与其阻滞Ｃａ２＋通道有关。

Using a circuit TV system and method of intracellular standard microelectrode,the effects of praeruptorin C on spontaneous contractile behavior and action Potential were observed in cultured myocardial cells of neonatal rats.There was a decline in both the contractile frequency and velocity of cell edge motion after exposure to Pra-C for 5 minutes. Pra-C(10 , 30 and 100 μmol·L-1)was shown to inhibit contraction velocity by 24%,43%and 51%, respectively in a concentration dependent manner.Pra-c(30 and 100μmol·L-1)inhibited the contractile frequency by 13%and 19%,respectively. Nifedipine 3 μmol·L-.shortened APD50 and APD90 by 14%and 17%but verapamil at the same concentration inhibited APA by 27%, shortened APD50 by 8%and prolonged APD90 and SCL by l0%and 43%, respectively. Pra-C10, 30 and 100μmol·L-1 shortened the APD50 by 7%,14%and l8%, respectively. Pra-C 30μmol·L-1 inhibited APA and prolonged SCL.The results suggest that the effects of Pra-C on cotractile behavior and action potential were related to its Ca2+ channel blockade.