内源性和外源性氧化可以防止血栓溶解后的冠状动脉内血栓和再封闭
S K Yao1, S Akhtar, T Scott-Burden
1Cullen Cardiovascular Research Laboratory, Texas Heart Institute, Houston, USA.
Circulation
|August 15, 1995
概括
氧化物 (NO) 的使用或补充在狗模型中延迟了冠状动脉内血栓的形成和重新封闭. 这表明NO可以抑制血小板聚合,为血栓形成提供潜在的治疗益处.
科学领域:
- 心血管研究研究心血管研究
- 药理学 药理学是指药理学的学科.
- 血液静止和血栓形成
背景情况:
- 氧化 (NO) 是血小板激活的关键调节剂.
- 了解NO在血栓形成中的作用对于心血管疾病管理至关重要.
研究的目的:
- 在犬模型中研究调节氧化 (NO) 水平对冠状动脉内血栓,血栓溶解和再封闭的影响.
- 评估NO合成酶抑制和NO捐献对血栓形成和血小板聚合的影响.
主要方法:
- 麻醉的狗接受了盐水,L-NNA (NO合成酶抑制剂),L-氨酸 (NO前体) 或SNP (NO捐赠体) 的冠心内注射.
- 冠内血栓形成是通过电刺激诱导的.
- 通过使用组织等离子体激活剂和肝素实现了血栓溶解.
- 评估了冠状动脉再封闭和活体血小板聚合.
主要成果:
- 与盐水和L-NNA相比,L-氨酸和SNP显著延长了血栓形成的时间.
- 血栓溶解成功率在所有组中都是相似的.
- 在用L-氨酸或SNP治疗的狗中,冠状动脉再封闭显著延迟.
- 活体血小板聚合被L-氨酸和SNP治疗抑制.
结论:
- 增加氧化 (NO) 产量或使用NO供体可以抑制血小板聚合.
- 调节NO水平可能是一个可行的策略,以延迟冠状动脉内血栓的形成,并防止血栓溶解后的再封闭.
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