Objective:To investigate the relationship of electrophysiological remodeling and arrhythmias via observing the alterations of QT interval and action potential duration(APD)in ventricular of diabetic rabbits in vivo.Method:Diabetes was induced by a single injection of alloxan(145mg/kg,i.v.)in rabbits.After the devel- opment of diabetes(10weeks),the main electrophysiological parameters and ventricular effective refractory period (ERP)as well as arrhythmias induced by program and burst-pacing electrical stimulation protocols were perfo- romed using ECG measurements and monophasic action potential recording in healthy and diabetic rabbits.Result: Compared with control group,heart rate was significantly retarded and QT interval was lengthened(all P0.05) in diabetic group.Moreover,ST segment was remarkedly altered upward and T amplitude was increased(all P 0.05)in diabetic group.The phases of AP of ventricular myocytes in diabetic rats were obviously wider than that in control rats.Compared with control group,the duration of AP at 10%,20%,and 50%level of repolarization (APD10,APD20and APD50)were significantly elongated in diabetic group(all P0.05).ERP was also obviously prolongated from (105.21±9.78)ms in control group to(168.95±10.03)ms in diabetic group(P0.05).Ven- tricular arrhythmias and/or fibrillation evens were markedly induced with occurrence of 87.5% by burst-pacing. Conclusion:The diabetic cardiomyopathys are significant vulnerabilities to ventricular arrhythmias,which is attrib- uted to severely electrophysiological remodeling in diabetic nullitus.
Objective To investigate the effects of diabetes on action potential(AP) and transient outward potassium current(Ito) in ventricular myocytes in rats.Methods Diabetes was induced by a single injection of streptozotocin(STZ,65 mg/kg,i.v.) in rats.At 14 weeks after STZ-treatment,AP and Ito were recorded via whole-cell patch clamp technique in enzymatically dissociated single rat ventricular myocytes coming from control and diabetic group.The dynamic curves of Ito were fitted by Boltzmann equations or biexponential function according to relationship between current densities and clamp voltage of Ito in contral and diabetic group.Results The phases of AP of ventricular myocytes in diabetic group were obviously wider than that in control group.Compared with control group,the AP duration(APD) at 20,50 and 90% level of repolarization(APD20,APD50 and APD90) were significantly elongated in diabetic group(64.3±7.5 ms vs 29.7±9.2 ms;174.3±6.8 ms vs 98.9±4.2 ms;276.7±8.3 ms vs 173.7±7.2 ms,all P0.01,n=12).With the +50 mV clamp potential,the current densities of Ito were significantly decreased from 17.43±1.98 pA/pF in control group to 11.51±1.37 pA/pF in diabetic group(P0.05,n=12).Compared with control group,The I-V curve of Ito was vitally suppressed downward,and the steady-state inactivation curve of Ito was significantly shifted to left(P0.01,n=12),as well as the recovery time of inactivation of Ito was markedly retarded in diabetic group.Conclusion APD of ventricular myocytes in diabetic rats is significantly prolongated,which is attributed to decrease of current densities of Ito,and acceleration of inactivation of Ito,as well as inhibition of recovery of inactivation of Ito in ventricular myocytes of diabetic rats.
Objective: To investigate the effects of ginkgo biloba extract(Egb761) on transient outward potassium current(Ito) and action potential of cardiomyocytes in rabbits,and to explore its ion channel mechanism in antagonizing ischemia-induced myocardial injury and arrhythmia.Methods: Cardiomyocytes from rabbit ventricle were obtained by enzymatic dissociation.The whole-cell patch-clamp technique was used to assess the effect of Egb761 on Ito and action potential.Results: ① With voltage clamp and administration of Egb761(60 μg/L),the current densities of Ito in cardiomyocytes significantly ascended in every commanding potential.When holding potential was-50 mV and commanding potential was +50 mV,the current densities of Ito were markedly increased from(7.59±0.19) pA/pF to(11.18±0.89) pA/pF with Egb761(60 μg/L) perfusion in 5 min(versus control,P0.01,n=8).Egb761 still maybe completely changed the I-V curve upward without changing the I-V curve direction.②According to current clamp protocol,action potentials recorded in control groups in rabbit cardiomyoytes consisted of five phases from upstroke to phase four.With administration of Egb761(60 μg/L),action potentials were shaped an acute triangle with rather shorter action potential durations(APD50 and APD90),which were obviously shortened from(83.6±4.3) ms to(51.3±3.2) ms and from(168.7±4.1) ms to(93.8±4.4) ms,respectively(versus control,P0.01,n=8,respectively).Conclusion: It suggests that Egb761 might increase Ito and shorten the action potential duration in cardiomyoytes.It might contribute to the protection of heart with ischemia and antiarrhythmia and increase heart function during the ischemic injury.
Objective To investigate the effects of baicalin on triggered activity(TA) arrhythmia Methods L-type calcium current(ICa-L) was recorded before and after baicalin via using whole-cell patch-clamp technique in enzymatically dissociated single rat ventricular myocytes. The transmembrane action potential(TAP) was performed before and after baicalin on rat papillary muscles by conventional glass microelectrode technique. Results ①With voltage clamp way,baicalin significantly inhibited ICa-L. The biggest current density of ICa-L was decreased from 15.8±1.2 pA/pF to 11.3±0.9,8.2±0.8 and 4.9±0.6 pA/pF respectively(all P0.01) by administration of baicalin (10,20 and 40μmol/L). Baicalin markedly blocked ICa-L with concentration-dependent relation with an IC50 value of 27.7±1.9μmol/L. Moreover,baicalin shifted the I-V curve of ICa-L upwards with voltage-dependent,but didn't change markedly the shape of I-V curve.②Baicalin (20μmol/L) significantly shortened ADP20,ADP50and APD90,but didn't apparently change other electrophysiological parameters of TAP in rat papillary muscles. Ouabain could apparently induced the delayed afterdepolarization(DAD) and TA under basic cycle length of 500 ms in rat papillary muscles. With addition of baicalin(20μmol/L),DAD and TA were markedly inclined,which was difficult to be revoked by ouabain (compared with ouabain group,P0.01). Conclusion Baicalin significantly inhibits ICa-L and ouabain-induced DAD and TA in rat hearts. It might be concerned about that baicalin blocked influx of ICa-L,and decreased Ca2+ overload in cardiomyocytes.
Objective: To study the effects of Lycium Barbarum polysaccharides(LBP) on L-type calcium channel current(ICa-L) in rat ventricular myocytes.Methods: Standard whole-cell patch clamp technique was used.Results: ①LBP could make the I-V curves upward.②LBP reduced the ICa-L in a concentration-dependent manner.③ LBP in the concentration of 50 mg/L made the steady-state activation curves shift to right,and increased the τ value of recovery duration obviously.But inactivation curve of ICa-L was not affected significantly.Conclusion: LBP could inhibit the L-type calcium channel,mainly acting on the activity and recovery processes.
Objective To investigate effects of propofol on action potential(AP) and L-type calcium channel curent(ICa-L) of subepicardial myocytes of both left and right ventricular walls of rabbits.Methods The subepicardial myocytes were obtained by enzymatic dissociation in left and right ventricular walls of rabbits.AP and ICa-L were recorded via whole-cell patch-clamp technique.Results According to current clamp protocol,APs which were recorded in subepicardial myocytes of both left and right ventricular walls consisted of five phases from upstroke to phase four,and were attached to a dome in the second plateau of the APs before propofol adminstration.Nonetheless,Propofol(250μmol/L) deleted the dome of the second plateau of the APs of subepicardial myocytes of left and right ventricular walls,which had not the second plateau and was shaped an acute triangle in APs of right subepicardial myocytes.Propofol significantly shortend the APD50 and APD90 in right and left subepicardium,and right subepicardium were more obvious during the voltage clamp protocol.Propofol(250μmol/L) significantly attenuated the peak amplitude of ICa-L and right subepicardium were more obvious those of that in left subepicardium(P0.01).Propofol shifted upward the I-V curve of ICa-L of both left and right subepicardial myocytes,but lifted outstandingly the I-V curve of ICa-L of right subepicardial myocytes on the top of all I-V curves. Conclusion Propofol attenuated more significantly on the APs and ICa-L of subepicardial myocytes of right ventricular wall than those of the same layer of left ventricular wall,so that induces cardiac electrical heterogeneity of subepicardial myocytes of both left and right ventricular walls.
Objective: To observe the effect of icariine on L-type calcium current in isolated rabbit ventricular myocytes by using whole-cell patch clamp technique.Methods: Single ventricular cell of rabbit was obtained by an enzymatic disassociation method.The whole-cell patch clamp technique was used to record the effect of icariine(ICA) on L-type calcium current(ICa,L) of rabbit ventricular myocytes.Results: ① 10,20 and 40 μmol/L ICA decreased peak Ica,L from(15.81±1.23) pA/pF to(11.27±0.89),(9.48±0.85) and(6.87±0.81) pA/pF,respectively(n=6,P0.05).Peak Ica,L was reduced by 28.7%,40.0% and 56.5%,respectively by ICA at 10,20 and 40 μmol/L.In addition,ICA could up-shift the I-V curves of ICa,L without changing their basic shape(n=6,P0.05);② 20 μmol/L ICA could delay the recovery time course of ICa,L from inactive state and cause inactivation curve moving leftward.Conclusion: ICA blocks ICa,L in a concentration-dependent manner,which may contribute to its anti-arrhythmia effect.