BACKGROUND:
Angiotensin Ⅱ-has been found to induce atrial electrical remodeling,which can be blocked or inhibited by allicin.OBJECTIVE:To
study the effects of allicin on
angiotensin Ⅱ-induced calcium channel current and
intracellular free calcium concentration in human atrial myocytes.DESIGN:A randomized controlled study based on human atrial myocytes freshly isolated.SETTING:Cardiology department of a military medical university of Chinese PLA.METHODS:This study was carried out from June 2003 to June 2004 in the Laboratory of Cardiology Department,Xijing Hospital,the Fourth Military Medical University of Chinese PLA.Ten patients with congenital heart disease who underwent extracorporeal circulation surgery were included in the study.Among them,there were 6 males and 4 females with the average age of 15± 6 years.Tissue samples were taken from their right auricle and sent to the lab,where the atrial myocytes were freshly isolated.There were four groups in the present study:① Control group:no intervention;② Angiotensin Ⅱ group:administration of angiotensin Ⅱ (0.1 μ mol/L);③ Allicin group:administration of allicin(50 μ mol/L);④ Angiotensin Ⅱ + allicin group:co administration of angiotensin Ⅱ (0.1 μ mol/L)and allicin(50 μ mol/L). The conventional whole-cell configuration of the patch clamp technique was used to detect membrane electric current of Ca2+ in L type.Confocal microscope was used with Fluo-3/AM as calcium indicator to detect changes of intracellular free calcium concentration immediately and 15 minutes after drug intervention,respectively.MAIN OUTCOME MEASURES:The peak density of electric current of Ca2+ in L type and alteration of fluoresence intensity of intracellular free calcium concentration.RESULTS:① Compared with that of control group,the peak density of electric current of Ca2+ in L type in human atrial myocytes was significantly increased by angiotensin Ⅱ of 0.1 μ mol/L<(- 12.77± 1.61) vs (- 5.78 ± 0.81) pA/pF,P< 0.05>.② Allicin of 50 μ mol/L did not significantly affect electric current of Ca2+ in L type in human atrial myocytes <(- 5.69± 0.83) pA/pF,P >0.05>.③ In angiotensin Ⅱ + allicin group,the peak density of electric current of Ca2+ in L type was significantly lower than that in angiotensin Ⅱ group<(- 8.75± 0.97) pA/pF,P< 0.05>.④ The alteration of intracellular fluoresence intensity of single cardiomyocyte in angiotensin Ⅱ group was significantly higher than that in control and allicin groups<(2 610.1± 112.6,(299.2± 27.3)% ; 653.9± 42.5,0;639.5± 44.7,(- 2.2± 0.6)% ,P< 0.05>.⑤ When allicin was added simultaneously with angiotensin Ⅱ ,the alteration of intracellular fluoresence intensity was much lower than that in angiotensin Ⅱ group<(1284.9± 85.2,(96.5± 8.4)% ;P< 0.05>.CONCLUSION:Allicin antagonizes angiotensin Ⅱ induced increase in the peak density of electric current of Ca2+ in L type and intracellular calcium overload, which may relieve atrial electrical remodeling.