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目的分析心房颤动(房颤)时心房肌组织醛固酮合成酶(CYP11B2),血管紧张素Ⅱ受体1、2(AT1、2-R)的变化与心房结构重构的关系。方法选择38例因心脏疾患需行外科手术的患者。按有无房颤病史分为3组,窦性心律组(SR,11例),阵发性房颤组(pAF,13例,房颤持续时间<6个月),持续房颤组(cAF,14例,房颤持续时间>6个月)。在非体外循环手术过程中切取右心耳组织约500 mg(持续房颤患者中有8例同时切取了左心耳组织500 mg)。采用聚合酶链反应测定心房肌组织 AT1-R、AT2-R、CYP11B2的表达,免疫组织化学观察 AT1-R 蛋白的分布。结果 cAF 组平均左房直径明显大于 SR 和 pAF 组(5.8 cm±0.6 cm,3.3 cm±0.4 cm;4.2 cm±0.7 cm,P<0.01)。cAF组的 AT1-R mRNA 表达水平比 SR 组明显降低(1.03±0.04和1.35±0.09,P<0.01)。AT2-R 的mRNA 表达水平比 SR 组明显上调(1.16±0.16和0.90±0.10,P<0.05)。CYP11B2的 mRNA 表达cAF 组与 pAF 组比 SR 组均明显增强(P<0.05～0.01)。结论 AT1-R mRNA 表达下调是对组织血管紧张素Ⅱ的过度反应,AT2-R mRNA 表达上调是对心房结构重构的适应和代偿反应。心房肌组织中的 CYP11B2 mRNA 表达增加。提示醛固酮可能参与了房颤患者的心房重构过程。
Objective To analyze the relationship between changes of aldosterone synthase (CYP11B2), angiotensin Ⅱ receptor 1 (AT1, 2-R) and atrial remodeling in atrial fibrillation (atrial fibrillation). Methods Thirty-eight patients undergoing surgery due to heart disease were selected. According to the presence or absence of atrial fibrillation, the patients were divided into 3 groups: sinus rhythm group (11 cases), paroxysmal atrial fibrillation group (13 cases, duration of atrial fibrillation <6 months) , 14 cases, duration of atrial fibrillation> 6 months). Approximately 500 mg of right atrial appendage tissue was excised during off-pump surgery (eight consecutive patients with atrial fibrillation and 500 mg of left atrial appendage). The expression of AT1-R, AT2-R and CYP11B2 in atrial myocardium was detected by polymerase chain reaction. The distribution of AT1-R protein was observed by immunohistochemistry. Results The average left atrial diameter of cAF group was significantly larger than that of SR and pAF group (5.8 cm ± 0.6 cm, 3.3 cm ± 0.4 cm; 4.2 cm ± 0.7 cm, P <0.01). AT1-R mRNA expression in cAF group was significantly lower than that in SR group (1.03 ± 0.04 and 1.35 ± 0.09, P <0.01). The mRNA expression of AT2-R was significantly up-regulated compared with SR group (1.16 ± 0.16 and 0.90 ± 0.10, P <0.05). CYP11B2 mRNA expression in cAF group and pAF group were significantly higher than those in SR group (P <0.05 ~ 0.01). Conclusions The down-regulation of AT1-R mRNA expression is an overreaction to tissue angiotensin Ⅱ. The up-regulation of AT2-R mRNA expression is an adaptive and compensatory response to atrial structural remodeling. CYP11B2 mRNA expression in atrial muscle tissue increased. Suggesting aldosterone may be involved in atrial fibrillation in patients with atrial remodeling process.