Hao Xiaojin, Månsson-Broberg Agneta, Blomberg Pontus, Dellgren Göran, Siddiqui Anwar J, Grinnemo Karl-Henrik, Wärdell Eva, Sylvén Christer
Department of Cardiology, Karolinska Institute and Karolinska University Hospital, Stockholm, Sweden.
Biochem Biophys Res Commun. 2004 Sep 10;322(1):292-6. doi: 10.1016/j.bbrc.2004.07.101.
Therapeutic angiogenesis is a potential treatment modality for myocardial ischemia. phVEGF-A(165), phPDGF-BB, or a combination of the two were injected into the myocardial infarct border zone in rats 7 days after ligation of the coronary left anterior descending artery. Cardiac function was measured by echocardiography. Hearts were harvested 1 and 4 weeks after plasmid injection. phVEGF-A(165) increased capillary density more than phPDGF-BB, and phPDGF-BB preferentially stimulated arteriolar growth. The combination increased both capillaries and arterioles but did not enhance angiogenesis any more than single plasmid treatments did. VEGF-A(165) and the combination of phVEGF-A(165) and phPDGF-BB counteracted left ventricular dilatation after 1 week but did not counteract further deterioration.
治疗性血管生成是心肌缺血的一种潜在治疗方式。在大鼠左冠状动脉前降支结扎7天后,将phVEGF-A(165)、phPDGF-BB或二者的组合注射到心肌梗死边缘区。通过超声心动图测量心脏功能。在注射质粒后1周和4周采集心脏。phVEGF-A(165)比phPDGF-BB更能增加毛细血管密度,且phPDGF-BB优先刺激小动脉生长。二者组合增加了毛细血管和小动脉数量,但在促进血管生成方面并不比单一质粒治疗效果更好。VEGF-A(165)以及phVEGF-A(165)与phPDGF-BB的组合在1周后可对抗左心室扩张,但无法对抗进一步的恶化。