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在心肌梗塞中诱导性氧化合成酶异酶的选择性调节
S M Wildhirt1, H Suzuki, D Horstman
1Department of Cardiac Surgery, Ludwig-Maximilians University, Munich, Germany. wildhirt@hch.med.uni-muenchen.de
Circulation
|October 7, 1997
概括
诱导性氧化合成酶 (iNOS) 的选择性抑制与SMT改善了心脏功能和心肌梗塞后的血流. 这表明iNOS有助于心脏病发作后的心脏功能障碍.
科学领域:
- 心血管科学 心血管科学
- 药理学 药理学是指药理学的学科.
- 生物化学 生物化学
背景情况:
- 诱导性氧化合成酶 (iNOS) 在心脏疾病中被激活.
- 增加iNOS活动可能会导致心肌梗塞后的左心室功能障碍.
研究的目的:
- 调查iNOS活动增加在心肌梗塞后左心室功能障碍中的作用.
- 评估选择性iNOS抑制对心脏表现和血流的影响.
主要方法:
- 新西兰的雄性子经历了心肌梗塞.
- 动物接受了盐水,S-甲基尿酸硫酸盐 (SMT) (选择性iNOS抑制剂) 或N(omega) -nitro-L-arginine (L-NNA) (非选择性NOS抑制剂) 的治疗.
- 测量包括NOS活性,血NOx,cGMP,血液动力学和心肌血流在不同的时间点.
主要成果:
- 心肌梗塞导致iNOS活动增加,心脏NOx产量增加,cGMP水平升高,但cNOS没有变化.
- 心脏病发作导致左心室功能受损 (增加LVEDP,减少dP/dt) 和心肌血流量减少.
- SMT选择性地抑制了iNOS,改善了左心室功能,并增加了心肌血流,而L-NNA具有更广泛的抑制作用和更糟糕的结果.
结论:
- 在心脏病发作后诱导的iNOS活动会产生负面的内效应,导致心肌功能障碍.
- 使用SMT选择性INOS抑制可以改善心脏性能和心肌血流.
- 针对iNOS活动可能是急性心肌梗塞的有益治疗策略.
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