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

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^-1)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。

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

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^-1.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.