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Basic science: Cardiovascular disease basic research
e0099 Baicalin protection rat cardiomyocytes from ischaemia-reperfusion injury and antiarrhythmia via inhibiting L-type calcium current
  1. Teng Wang,
  2. Jingjing Wang,
  3. Wenyun Gan,
  4. Congxin Huang
  1. Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute of Wuhan University, Wuhan, China

Abstract

Objective To investigate baicalin protection rat cardiomyocytes from inschemia-reperfusion injury and antiarrhythmia via blocking ICa-L.

Methods The degree of ischaemia-reperfusion injury was assessed by the recovery of LVDP and the magnitude of the reperfusion contracture with using approach of the Langendorff-perfused isolated rat hearts. The effects of baicalin on APs and ouabain-induced DAD and AT were performed on rat papillary muscles by conventional microelectrode technique. ICa-L was recorded via using whole-cell patch-clamp technique in enzymatically dissociated single rat ventricular myocytes.

Results Compared with the pre-ischaemic control, baicalin could concentration-dependently improved recovery of LVDP, and reduced the lever of reperfusion contracture, and occurrence of arrhythmias. Baicalin significantly shortened ADP20, ADP50 and APD90 in rat papillary muscles. Ouabain could apparently induced the DAD and TA in rat papillary muscles. With administration of baicalin, the electrophysiological parameters of ouabain-induced DAD and TA were markedly inclined to difficult occurrence. It illustrated that baicalin might inhibit influx of ICa-L. Baicalin significantly inhibited ICa-L in a voltage-dependent and concentration-dependent procedure, with an IC50 value of 27.7±1.9 μmol/l (Emax and nH were 115.2±3.3% and 1.07±0.05, respectivly). Moreover, baicalin shifted the I-V curve of ICa-L upwards. According to statistic kinetic data, it was suggested that baicalin especially inhibit the ICa-L by eliciting a negative shift of the steady-state inactivation without affecting the slop factor. To the effect of baicalin on the speed of ICa-L recovery from inactivation, our data indicated that the time courses of recovery were prolonged markedly (p<0.01 compare with control group, respectively).

Conclusions Baicalin improved cardioprotection effects on ischaemia-reperfusion injury and decreased the occurrence of ouabain-induced DAD and TA, thus inhibited ICa-L. The effects of baicalin on inhibiting ICa-L might contribute to baicalin antagonising ischaemia-reperfusion injury and arrhythmia.

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