| In vitro: |
| Am J Chin Med. 2010;38(1):37-49. | | Daurisoline suppressed early afterdepolarizations and inhibited L-type calcium current.[Pubmed: 20128043] | Our previous studies have shown that Daurisoline (DS) exerted antiarrhythmic effects on various experimental arrhythmias. In this study, the effects of Daurisoline on early afterdepolarizations (EADs) and its possible mechanisms have been investigated. Cardiac hypertrophy was induced in rabbits by coarctating the abdominal aorta.
METHODS AND RESULTS:
The effects of Daurisoline on action potential duration (APD) and the incidences of EADs were studied in hypertrophied papillary muscles of rabbits in the conditions of low external K(+) concentration ([K(+)]o) and dofetilide (dof) by using standard microelectrode technique. The whole-cell patch clamp was used to record the L-type calcium current (I(Ca-L)) in isolated left ventricular cells of rabbits. The results showed that in hypertrophied papillary muscles of rabbits with low [K(+)]o ([K(+)]o = 2.7 mM), 1 microM dof prolonged APD(50) and APD(90) markedly and the incidence of EADs was 66.7% (4/6, p < 0.01); when 15 microM Daurisoline was applied, the incidence of EADs was 0% (0/4, p < 0.01) and the prolonged APD was shortened (p < 0.01). In a single myocyte, Daurisoline could also inhibit EADs induced by dof, low [K(+)]o and low external Mg(2+) concentration ([Mg(2+)]o) ([Mg(2+)](o) = 0.5 mM). Daurisoline could decrease the triangulation. In a single myocyte, Daurisoline could make the I-V curve upward, shift the steady-state activation curves to the right and the steady-state inactivation curves to the left and prolong the tau value of recovery curve obviously.
CONCLUSIONS:
These results suggested that Daurisoline could inhibit EADs which may be associated with its blockade effects on I(Ca-L). | | Zhongguo Yao Li Xue Bao. 1996 May;17(3):248-51. | | Effects of daurisoline on intracellular Ca2+ activity in myocardium.[Pubmed: 9812749] | To explain the effect of daurisoline (DS) on delayed afterdepolarization (DAD).
METHODS AND RESULTS:
Ca(2+)-sensitive microelectrode technic was used to record intracellular Ca2+ activity (alpha Cai) and triggered activity (TA) arising from DAD in myocardium.
Strophantin G 3 mumol.L-1 yielded an increase in resting myocardial alpha Cai by 0.19 +/- 0.11 mumol.L-1 and transient elevations of alpha Cai by 1.48 +/- 0.55 and 4.96 +/- 1.81 mumol.L-1, respectively during the development of DAD and TA. By pretreatment with DS or verapamil, strophantin G-caused elevations of the alpha Cai in resting and provoked myocardia were eliminated and TA disappeared. DS 50 mumol.L-1 reduced Na(+)-free medium-induced elevation of dog Purkinje fibrous alpha Cai and abolished caffeine-induced increase of dog myocardial alpha Cai.
CONCLUSIONS:
DS inhibited DAD and TA by preventing an increase of alpha Cai via transmembrane Ca2+ entry and Ca2+ release from the reticulum. |
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