ангиотензин II 受体阻塞降低了动脉冲动引起的心房粘附分子表达
Andreas Goette1, Alicja Bukowska, Uwe Lendeckel
1Division of Cardiology, Otto von Guericke University Hospital Magdeburg, Magdeburg, Germany. andreas.goette@med.ovgu.de
Circulation
|January 30, 2008
概括
心房动 (AF) 和心率加快会增加心脏组织中的血管细胞粘附分子-1 (VCAM-1). ангиотензин II 受体抑制剂可以降低这种 VCAM-1,这表明它在预防血凝块方面发挥着作用.
科学领域:
- 心脏病学 心脏病学
- 血管生物学 血管生物学
- 分子医学是分子医学.
背景情况:
- 炎症标志物预测心房动 (AF) 中的血栓栓塞事件.
- 像VCAM-1和ICAM-1这样的内心粘附分子可能会将炎症与AF中的前血栓机制联系起来.
- 这一过程有助于血栓发育和心房内心脏重塑.
研究的目的:
- 为了研究AF患者心房组织中原血栓蛋白的表达.
- 为了确定快速心房节奏对体外和体内VCAM-1表达的影响.
- 评估 ангиотензин II 受体阻断对刺激诱导的 VCAM-1 上调调节的治疗效果.
主要方法:
- 组织微阵列分析了320名AF患者的右心房样本.
- 评估VCAM-1,ICAM-1和其他蛋白质的表达是通过免疫组织化学和西式涂抹.
- 实验室人类心房组织和体内猪模型被用于研究快速心房节奏效应和血管酶二受体阻塞 (奥梅沙坦,伊尔贝沙坦).
主要成果:
- 与对照组相比,AF患者的VCAM-1表达强度显著增加.
- 快速心房节奏 in vitro 和 in vivo 导致VCAM-1 的上调.
- 用olmesartan (体外) 和irbesartan (体内) 阻断 ангиотензинII受体消除了节奏诱导的VCAM-1表达.
- VCAM-1上调在左心室比右心室更为明显.
结论:
- 无论是AF还是快速心房节奏都会增加内心VCAM-1表达.
- ангиотензинII受体阻塞有效地减弱了这种VCAM-1的增加.
- 这些发现支持血管新生素II在AF期间的前血栓内心重塑中的病理生理学作用.
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