Objective Allocryptopine （ALL） is an effective alkaloid of Corydalis decumbens （Thunb.） Pers. Papaveraceae and has proved to be an- ti-arrhythmic. The purpose of our study is to investigate the effects of ALL on t...Objective Allocryptopine （ALL） is an effective alkaloid of Corydalis decumbens （Thunb.） Pers. Papaveraceae and has proved to be an- ti-arrhythmic. The purpose of our study is to investigate the effects of ALL on transmural repolarizing ionic ingredients of outward potassium current （Ito） and slow delayed rectifier potassium current （IKs）. Methods The monophasic action potential （MAP） technique was used to record the MAP duration of the epicardium （Epi）, myocardium （M） and endocardium （Endo） of the rabbit heart and the whole cell patch clamp was used to record/to and IKs in cardiomyocytes of Epi, M and Endo layers that were isolated from rabbit ventricles. Results The effects of ALL on MAP of Epi, M and Endo layers were disequilibrium. ALL could effectively reduce the transmural dispersion of repolarization （TDR） in rabbit transmural ventricular wall. ALL decreased the current densities of/to and IKs in a voltage and concentration dependent way and narrowed the repolarizing differences among three layers. The analysis of gating kinetics showed ALL accelerated the channel activation ofIto in M layers and partly inhibit the channel openings of/to in Epi, M and Endo cells. On the other hand, ALL mainly slowed channel deactivation of IKs channel in Epi and Endo layers without affecting its activation. Conclusions Our study gives partially explanation about the mechanisms of tmnsmural inhibition of/to and IKs channels by ALL in rabbit myocardium. These findings provide novel perspective regarding the anti-arrhythmogenesis application of ALL in clinical settings.展开更多
Objective： To investigate stretch-induced electrophysiological changes in chronically infarcted hearts and the effect of streptomycin （SM） on these changes in vivo. Methods： Sixty Wistar rats were divided randomly...Objective： To investigate stretch-induced electrophysiological changes in chronically infarcted hearts and the effect of streptomycin （SM） on these changes in vivo. Methods： Sixty Wistar rats were divided randomly into four groups： a control group （n=15）, an SM group （n=15）, a myocardial infarction （MI） group （n=15）, and an MI＋SM group （n=15）. Chronic MI was obtained by ligating the left anterior descending branch （LAD） of rat hearts for eight weeks. The in vivo blockade of stretch-activated ion channels （SACs） was achieved by intramuscular injection of SM （180 mg/（kg·d）） for seven days after operation. The hearts were stretched for 5 s by occlusion of the aortic arch. Suction electrodes were placed on the anterior wall of left ventricle to record the monophasic action potential （MAP）. The effect of stretching was examined by assessing the 90% monophasic action potential duration （MAPD90）, premature ventricular beats （PVBs）, and ventricular tachycardia （VT）. Results： The MAPD90 decreased during stretching in both the control （from （50.27±5.61） ms to （46.27±4.51） ms, P〈0.05） and MI groups （from （65.47±6.38） ms to （57.47±5.76 ms）, P〈0.01 ）. SM inhibited the decrease in MAPD90 during inflation （（46.27±4.51） ms vs. （49.53±3.52） ms, P〈0.05 in normal hearts; （57.47±5.76） ms vs. （61.87±5.33） ms, P〈0.05 in MI hearts）. The occurrence of PVBs and VT in the MI group increased compared with that in the control group （PVB： 7.93±1.66 vs. 1.80±0.86, P〈0.01; VT： 7 vs. 1, P〈0.05）. SM decreased the occurrence of PVBs in both normal and MI hearts （0.93±0.59 vs. 1.80±0.86 in normal hearts, P〈0.05; 5.40±1.18 vs. 7.93±1.66 in MI hearts, P〈0.01）. Conclusions： Stretch-induced MAPD90 changes and arrhythmias were observed in chronically infarcted myocardium. The use of SM in vivo decreased the incidence of PVBs but not of VT. This suggests that SACs may be involved in mechanoelectric feedback （MEF）, but that there might be other mechanisms involved in causing VT in chronic MI.展开更多
文摘Objective Allocryptopine （ALL） is an effective alkaloid of Corydalis decumbens （Thunb.） Pers. Papaveraceae and has proved to be an- ti-arrhythmic. The purpose of our study is to investigate the effects of ALL on transmural repolarizing ionic ingredients of outward potassium current （Ito） and slow delayed rectifier potassium current （IKs）. Methods The monophasic action potential （MAP） technique was used to record the MAP duration of the epicardium （Epi）, myocardium （M） and endocardium （Endo） of the rabbit heart and the whole cell patch clamp was used to record/to and IKs in cardiomyocytes of Epi, M and Endo layers that were isolated from rabbit ventricles. Results The effects of ALL on MAP of Epi, M and Endo layers were disequilibrium. ALL could effectively reduce the transmural dispersion of repolarization （TDR） in rabbit transmural ventricular wall. ALL decreased the current densities of/to and IKs in a voltage and concentration dependent way and narrowed the repolarizing differences among three layers. The analysis of gating kinetics showed ALL accelerated the channel activation ofIto in M layers and partly inhibit the channel openings of/to in Epi, M and Endo cells. On the other hand, ALL mainly slowed channel deactivation of IKs channel in Epi and Endo layers without affecting its activation. Conclusions Our study gives partially explanation about the mechanisms of tmnsmural inhibition of/to and IKs channels by ALL in rabbit myocardium. These findings provide novel perspective regarding the anti-arrhythmogenesis application of ALL in clinical settings.
基金Project supported by the National Natural Science Foundation of China(No.81301343)
文摘Objective： To investigate stretch-induced electrophysiological changes in chronically infarcted hearts and the effect of streptomycin （SM） on these changes in vivo. Methods： Sixty Wistar rats were divided randomly into four groups： a control group （n=15）, an SM group （n=15）, a myocardial infarction （MI） group （n=15）, and an MI＋SM group （n=15）. Chronic MI was obtained by ligating the left anterior descending branch （LAD） of rat hearts for eight weeks. The in vivo blockade of stretch-activated ion channels （SACs） was achieved by intramuscular injection of SM （180 mg/（kg·d）） for seven days after operation. The hearts were stretched for 5 s by occlusion of the aortic arch. Suction electrodes were placed on the anterior wall of left ventricle to record the monophasic action potential （MAP）. The effect of stretching was examined by assessing the 90% monophasic action potential duration （MAPD90）, premature ventricular beats （PVBs）, and ventricular tachycardia （VT）. Results： The MAPD90 decreased during stretching in both the control （from （50.27±5.61） ms to （46.27±4.51） ms, P〈0.05） and MI groups （from （65.47±6.38） ms to （57.47±5.76 ms）, P〈0.01 ）. SM inhibited the decrease in MAPD90 during inflation （（46.27±4.51） ms vs. （49.53±3.52） ms, P〈0.05 in normal hearts; （57.47±5.76） ms vs. （61.87±5.33） ms, P〈0.05 in MI hearts）. The occurrence of PVBs and VT in the MI group increased compared with that in the control group （PVB： 7.93±1.66 vs. 1.80±0.86, P〈0.01; VT： 7 vs. 1, P〈0.05）. SM decreased the occurrence of PVBs in both normal and MI hearts （0.93±0.59 vs. 1.80±0.86 in normal hearts, P〈0.05; 5.40±1.18 vs. 7.93±1.66 in MI hearts, P〈0.01）. Conclusions： Stretch-induced MAPD90 changes and arrhythmias were observed in chronically infarcted myocardium. The use of SM in vivo decreased the incidence of PVBs but not of VT. This suggests that SACs may be involved in mechanoelectric feedback （MEF）, but that there might be other mechanisms involved in causing VT in chronic MI.
