The effect of allicin on the ventricular myocytes of rabbit with heart failure

Abstract

Objective To observe the effect of allicin on the action potential duration (APD) and L-type calcium current (ICa, L) in the ventricular myocytes of rabbits with heart failure in order to explore the mechanisms of therapeutic effect of allicin on cardiac arrhythmias complicated with heart failure. Methods Forty-five New Zealand White male rabbits were randomly (random number) assigned to 3 groups (n=15 in each group): sham operated group (sham group), heart failure group (HF group), and heart failure treated with allicin group (HF+All group). The rabbit heart failure model was established by abdominal aortic constriction coupled with aortic regurgitation, the ventricular myocytes were obtained by enzyme double digestion, and the whole cell clamp was used to record action potential and calcium current.The action potential duration (APD), ICa, L and gating mechanism were observed during heart failure and allicin administered. Data were processed with pCLAMP version 10.2. Statistical analysis was performed using SPSS 17.0. Comparisons among groups were carried out using ANOVA, and SNK-q was used for multiple comparison as post-hoc. Results (1) Prolonged APD was found during heart failure, APD50 was prolonged from (93.4±4.7) ms in sham group to (115.5±6.2) ms in HF group(P<0.01). After administration of allicin 30 μmol/L, APD50 was shortened to (105.2±5.5) ms (P<0.05). (2) The density of ICa,L increased during heart failure, peak current density increased increased from (-8.4±0.6) pA/pF in sham group to (-15.1±1.1) pA/pF while 0 mV attained at depolarizations (P<0.01). After administration of allicin 30 μmol/L, the current density reduced to (-10.1±0.8) pA/pF ( P<0.01). The effect of allicin presented in both voltage dependent and consentration dependent manner. (3) According to the gating mechanism study, the main mechanism of lowering the density of ICa, L by allicin after heart failure was the acceleration of the steady inactivation of the channel, and the de-escalation of the recovery kinetic after the inactivation of the channel. Conclusions Allcin can be used to reduce the calcium current of ventricular myocytes in animal heart failure model, it has the potential of clinical use in treating cardiac arrhythmias during heart failure. Key words: Allicin; Heart failure; Rabbit; Ventricular myocytes; Action potential; L- calcium current