卡托普利对家兔快速心房起搏所致电重构的作用及其机制

Effect of Captopril on tachycardia-induced electrical remodeling of rabbit atria and its mechanism

目的 :观察血管紧张素转换酶抑制剂卡托普利对家兔快速心房起搏所致电重构的作用 ,探讨其防治房颤的机制。方法 :家兔 32只随机分为 3组 :对照组 8只 ,快速起搏组和卡托普利组各 12只。经颈内静脉将电极置入右心房 ,分别测定各组基础状态、给药后 0 .5 h和以 6 0 0次 / m in行快速心房起搏后 0 .5、1、2、4、6、8h的心房有效不应期(AERP2 0 0 、AERP1 50 和 AERP1 30 ) ,用生化方法检测心肌组织内 Ca2 + 含量。结果 :快速心房起搏后快速起搏组的AERP缩短 ,AERP的频率适应不良 ,同起搏前比较差异显著 (P<0 .0 1) ,心肌组织内 Ca2 +含量升高 (P<0 .0 1) ,而卡托普利组 AERP缩短较快速起搏组减轻 ,AERP频率适应性得以维持 ,心肌组织 Ca2 +含量低于快速起搏组 (P<0 .0 5 )。结论 :心房肌组织内钙含量的升高在快速起搏导致的心房电重构中起一定作用 ,卡托普利能减轻钙超载而抑制快速心房起搏所致电重构。

AIM: To investigate the effects of angiotensin-converting enzyme inhibitor (ACEI) Captopril on electrical remodeling (ER) of the atrium induced by rapid atrial pacing in rabbits and to explore the mechanism of therapeutic effects of ACEI on atrial fibrillation (AF). METHODS: 32 rabbits were randomely divided into 3 groups: control group (n=8), rapid pacing group (n=12) and Captopril group (n=12). Atrial effective refractory period (AERP) was measured by programmed electrical stimulation before pacing and from 0 to 8 hours after the onset of the pacing. Ca 2+ content of atrial tissues was assessed by biochemical technique. RESULTS: The AERP was shortened and the rate adapation of AERP was lost through the pacing process compared with those before pacing (P<0.01), Ca 2+ content was increased in rapid pacing group than in control group(P<0.01). The shortening of AERP was attenuated, the rate adapation was maintained, and the content of Ca 2+ in Captopril group was less than in rapid pacing group(P<0.05). CONCLUSION: The ER of the atrium is at least in part mediated by an increased calcium content in the atrial tissues during prolonged rapid atrial pacing. ACEI can decrease the extent of ER by way of inhibiting Ca 2+ overload.