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通过下肢缺血症的重血管化逆转血管生长因子上调的逆转
Paolo Porcu1, Costanza Emanueli, Maria Kapatsoris
1Institute of Internal Medicine, Medical University of Sassari, Sassari, Italy.
Circulation
|January 5, 2002
概括
在慢性外周血管疾病中,组织kallikrein (tK) 被上调,可能有助于血液流动. 血管内皮生长因子 (VEGF) 水平保持不变. 在重血管化手术后,tK水平正常化.
科学领域:
- 血管生物学 血管生物学
- 血管新生研究研究
- 生物标志物发现发现
背景情况:
- 组织卡利克莱因 (tK) 和血管内皮生长因子 (VEGF) 是已知的血管生成剂.
- 在急性缺血动物模型中观察到tK或VEGF的升调.
- 这些线粒原体在慢性外周血管功能不全中所起的作用尚不清楚.
研究的目的:
- 在患有症状的外周血管疾病的患者中研究循环tK和VEGF的表达.
- 为了确定tK和VEGF水平在手术重血管化前后是否发生变化.
- 探索tK水平与附带船舶形成之间的相关性.
主要方法:
- 在外科手术前后对36名患有外周血管疾病的患者进行循环tK和VEGF测量.
- 在6名患者的运动压力测试中测试的tK.
- 从缺血性四肢分析了tK水平的静脉排泄物,并与血管学数据相关联.
主要成果:
- VEGF水平处于正常范围内,在再血管化后没有变化.
- 与对照组相比,36名患者中34名患者的tK上调 (P<0.05).
- tK水平与附带血管数 (P<0.001) 和恢复血管后正常化 (P<0.01) 呈正相关性.
结论:
- tK诱导可能是慢性动脉衰竭的补偿机制,促进组织输液.
- 像tK和VEGF这样的生长因子的差异表达对治疗性血管生成有影响.
- tK 作为外周血管功能不充分和治疗反应的潜在生物标志物.
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