摘要
目的探讨咪达普利(IMI)对家兔左室肥厚心肌(LVH)内向整流钾电流(IK1)的跨室壁不均一性的影响。方法用腹主动脉缩窄法制备家兔LVH模型,并口服IMI[0.625mg/(kg·d)]连续8周进行干预。取心脏分离左室游离壁3层心肌细胞,用全细胞膜片钳技术记录IK1。结果因LVH模型心肌细胞膜电容增加所致IK1密度明显减少,心外膜下心肌、中层心肌和心内膜下心肌分别从(5.9±0.7)pA/pF、(6.1±0.5)pA/pF和(4.9±0.3)pA/pF降低为(4.4±0.5)pA/pF、(4.5±0.4)pA/pF和(2.1±0.2)pA/pF,各层细胞间电流密度差异加大。IMI处理后,可逆转心肌的病变,IK1的密度明显高于IMI未干预的LVH组(P<0.05),心外膜下心肌、中层心肌和心内膜下心肌分别为(5.4±0.8)pA/pF、(5.8±0.6)pA/pF和(4.3±0.5)pA/pF,使3层细胞间电流密度的差异减小。结论IMI可逆转LVH后心肌细胞IK1的改变,减少跨室壁差异,提示可能是其减少LVH后发生快速心律失常的机制之一。
AIM To evaluate the effect of imidapril on transmural heterogeneity of inward rectifier potasslum current （ IK1 ） of myocytes in rabbits with left ventricle hypertrophy （LVH）. METHODS LVH model was induced by partial ligation of abdominal aorta of rabbit and IMI [ 0. 625 mg/（ kg · d） ] was orally administered for 8 weeks. Subepicardium （ Epi）, midmyocardium （M） and subendocardium （Endo） were isolated from the left ventricular free wall in rabbits and inward rectifier potassium current was recorded with whole-cell patch clamp way. RESULTS With the increment of cellular membrane capacitance in LVH cells, [KI densities of Endo, M and Epi decreased from （5.9 ±0. 7） pA/pF, （6. 1 ±0. 5） pA/pF and （4.9 ± 0. 3 ） pA/pF in normal cells to （4. 4 ± 0. 5 ） pA/pF, （4. 5 ± 0. 4 ） pA/pF and （2. 1 ± 0. 2） pA/pF in LVH cells. The difference of current densities between three layer ceils significantly increased （P 〈 0.05）. The IKL densities of treatment group with IMI increased to （5.4 ± 0. 8 ） pA/pF （ Epi）, （5.8 ± 0. 6） pA/pF （M） and （4. 3 ± 0.5 ） pA/pF （Endo）. Furthermore, the diversity of IK1 densities of Epi, M and Eudo was reduced significantly （P 〈0. 05）. CONCLUSION These results suggest that IMI can decrease transmural heterogeneity of inward rectifier potassium current of LVH myocytes in rabbits, which might be responsible for the antiarrhythmias effects of IMI.
出处
《心脏杂志》
CAS
2008年第6期663-667,共5页
Chinese Heart Journal
关键词
咪达普利
心肌肥厚
内向整流钾电流
异质性
imidapril
hypertrophy
inward rectifier potassium current
transmural heterogeneity
