中文摘要：

目的：探讨阿利吉仑及贝那普利对犬快速心房起搏心房离子通道重构的影响。方法健康成年杂种犬24只，分为4组：假手术组（ S 组），心房起搏对照组（ C 组），心房起搏＋阿利吉仑10 mg· kg－1· d－1组（ A组），心房起搏＋贝那普利4 mg· kg－1· d－1组（ B组）。每组6只。 S组植入起搏器，不行起搏刺激及药物干预。 C组植入起搏器并起搏，无药物干预。 A组及B组分别于起搏开始前3 d开始给予口服阿利吉仑10 mg· kg－1· d－1及贝那普利4 mg· kg－1· d－1直至实验结束。各组犬经500次／min快速心房起搏2周。胶原酶法分离左心房肌细胞行全细胞电流记录，观察各组犬L型钙通道电流（ICaL）、钠通道电流（INa）的电流密度变化，ICaLα1C亚单位（Cav1．2）及INav1．5 a亚单位（Nav1．5 a ）在心房组织基因水平的表达。结果快速心房起搏2周后，C组犬心肌细胞Cav1．2及Nav1．5 a蛋白表达水平的下降，ICaL、INa电流密度亦显著下降。 B组ICaL、INa电流密度显著高于C组。 B ∶C：[ICaL：－6．31±1．68对－3．72±2．15电流密度／电流强度（pA／pF）；INa：－62．32±21．68对－29．27±9．87 pA／pF，均 P＜0．01]。 A组不能预防起搏后ICaL电流的降低与C组无区别（P＞0．05）。 C组Cav1．2及Nav1．5 a蛋白表达水平下降。 A、B组均能预防起搏后Cav1．2及Nav1．5 a蛋白表达水平的下降，A组较B组Cav1．2蛋白表达水平差异无统计学意义（ P＞0．05）。 A组和B组均可以预防起搏诱发的Nav1．5α蛋白表达的下降，且逆转蛋白表达的幅度，B组要优于A组（B ∶A：0．903对0．597，P＜0．05）。结论阿利吉仑、贝那普利可能是通过对Na、Ca通道的基因表达的影响，逆转快速心房起搏引起的心房离子通道重构的变化。阿利吉仑、贝那普利可能对Na、Ca通道的基因表达及离子通道重构差异无统计学意义。

英文摘要：

Objective To investigate the effects of aliskiren and benazepril on atrial electrical remode-ling in a canine model of rapid atrial pacing .Methods Twenty-four dogs were assigned to sham （S）,control paced （C）,paced＋aliskiren （10 mg· kg-1· d-1,A）,paced and benazepril （4 mg· kg-1· d-1,B） group. Six dogs in each group.Rapid atrial pacing at 500 beats per minute was maintained for 2 weeks,but dogs in sham group were instrumented without pacing .During the pacing ,aliskiren （ 10 mg· kg-1· d-1 ,A） and benaze-pril （ 4 mg· kg-1· d-1 ,B） were given orally .Whole-cell patch-clamp technique was used to record atrial L-type calcium current（ICaL） and sodium channel current （INa） ionic currents.Collagenase was used for atrial cell isolation.Western-Blotting and RT-PCR were applied to assess atrial protein expression levels of ICaLα1C and INaV1.5αsubunits.Results Compared with S group,the density of ICaL and INa currents was significantly re-duced in atrial cells from paced dogs （ P〈0.05）.The density of INa currents in the group A was significantly higher than that in the pacing-control group （P〈0.05）.The density of ICaL and INacurrents in the group B was significantly higher than that in the pacing-control group （ B∶C：ICaL：-6.31±1.68 vs.-372±2.15 pA/pF;INa：-62.32±21.68 vs.-29.27±9.87 pA/pF：P〈0.05）.The protein levels of ICaLα1C （Cav1.2） and INaV1.5 （Nav1.5α） decreased in the pacing-control group compared with the sham-operated group （P〈0.01）.The pro-tein levels of Cav1.2 and Nav1.5αin A and B groups were higher than that in C group （P〈0.01）.There was no difference in Cav1.2 protein levels between A and B group （P〉0.05）.The protein levels of Nav1.5αin B group were higher than that in A group （B∶A：0.903 vs.0.597,P〈0.05）.Conclusion These results suggest that aliskiren and benazepril have differing influences on atrial tachycardia -induced atrial ionic remodeling .