Department of Internal Medicine, Chang Gung University College of Medicine, Kaohsiung Hsien 83301, Taiwan, Republic of China.
Cardiovasc Pathol. 2011 Mar-Apr;20(2):99-106. doi: 10.1016/j.carpath.2009.12.005. Epub 2010 Jan 18.
Oxidative stress is linked with several cardiovascular diseases. However, the NADPH oxidase activity in severe mitral regurgitation patients with and without atrial fibrillation has not yet been explored.
This study involved 16 adult patients (eight patients with persistent atrial fibrillation and eight with sinus rhythm) with severe mitral and moderate-to-severe tricuspid regurgitation and five control patients without mitral and tricuspid disease. Atrial tissues of the right and left atrial appendages were obtained during surgery. Superoxide anion production was measured by lucigenin-enhanced chemiluminescence, and the expression of nox2 containing NADPH oxidase mRNA was measured by quantitative real-time RT-PCR. Additionally, immunohistochemical study was performed.
NADPH-stimulated superoxide release was significantly higher than basal superoxide production from right [5671.9±3498.7 vs. 232.7±70.0 relative light units per second per milligram of protein (RLU s(-1) mg protein(-1)), P=.008) and left atrial homogenates (6475.1±1890.8 vs. 229.0±79.6 RLU s(-1) mg protein(-1), P=.008) in atrial fibrillation patients. The NADPH-stimulated superoxide release from right atrial homogenates was also significantly higher than basal superoxide production in sinus patients (6809.1±1327.1 vs. 244.2±65.5 RLU s(-1) mg protein(-1), P=.008). Additionally, there was a borderline significant correlation between NADPH-stimulated superoxide production from left atrial homogenates and left atrial sizes (r=0.683, P=.062) in atrial fibrillation patients. Membrane-bound nox2 containing NADPH oxidase mRNA expression was increased and was similar in both the atrial fibrillation patients and sinus patients. The NADPH-stimulated superoxide production in right atrial homogenates in control atrial samples was 1863.7±137.2 RLU s(-1) mg protein(-1). Immunohistochemical study demonstrated increased expression of nox2 in myocytes with moderate-to-severe myolysis and hypertrophy.
Results of this study demonstrate that membrane-bound nox2 containing NADPH oxidase activity and expression in the atrial myocardium is increased in patients with severe mitral regurgitation, possibly contributing to atrial remodeling in this clinical setting.
氧化应激与多种心血管疾病有关。然而,尚不清楚伴有或不伴有心房颤动的重度二尖瓣反流患者的 NADPH 氧化酶活性如何。
本研究纳入了 16 名成年患者(8 名持续性心房颤动患者和 8 名窦性节律患者),他们患有重度二尖瓣和中重度三尖瓣反流,以及 5 名无二尖瓣和三尖瓣疾病的对照患者。在手术期间获取右心房和左心耳的心房组织。通过荧光素酶增强化学发光法测量超氧阴离子的产生,通过实时定量 RT-PCR 测量含 NADPH 氧化酶的 nox2 mRNA 的表达。此外,还进行了免疫组织化学研究。
NADPH 刺激的超氧释放明显高于右心房[5671.9±3498.7 比 232.7±70.0 相对光单位每秒每毫克蛋白(RLU s(-1) mg protein(-1))]和左心房匀浆(6475.1±1890.8 比 229.0±79.6 RLU s(-1) mg protein(-1))(P=.008)]的基础超氧产生。在心房颤动患者中,NADPH 刺激的右心房匀浆超氧释放也明显高于窦性患者的基础超氧产生(6809.1±1327.1 比 244.2±65.5 RLU s(-1) mg protein(-1),P=.008)。此外,在心房颤动患者中,NADPH 刺激的左心房匀浆超氧产生与左心房大小呈边缘显著相关(r=0.683,P=.062)。膜结合含 NADPH 氧化酶的 nox2 mRNA 表达增加,在心房颤动患者和窦性患者中相似。在对照心房样本的右心房匀浆中,NADPH 刺激的超氧产生为 1863.7±137.2 RLU s(-1) mg protein(-1)。免疫组织化学研究表明,中度至重度肌溶解和肥大的心肌细胞中 nox2 的表达增加。
本研究结果表明,在重度二尖瓣反流患者的心房心肌中,膜结合的含 NADPH 氧化酶的 nox2 活性和表达增加,可能导致这种临床情况下的心房重构。