Vascular endothelial growth factor administration in chronic myocardial ischemia
Vascular endothelial growth factor administration in chronic myocardial ischemia
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DOI：
10.1152/ajpheart.1996.270.5.h1791
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发表时间：
1996-05-01
影响因子：
4.8
通讯作者：
Simons, M
中科院分区：
文献类型：
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作者：
Harada, K;Friedman, M;Simons, M
血管内皮生长因子（VEGF）是一种能够刺激血管生成的有丝分裂原。我们研究了VEGF给药在慢性猪心肌缺血模型中的作用。19头猪用近端左回旋支冠状动脉（LCX）Ameroid缩窄器进行器械固定。在8只动物中，用渗透泵将VEGF（2 μ g）和肝素（50 U）腔外给予LCX心肌4周，11只其它动物作为对照。VEGF治疗的动物在静息和起搏期间的LCX区域中的血流均高于未治疗的对照组（静息：1.35 +/- 0.1 vs. 0.80 +/- 0.09 ml . min（-1）。g（-1）;起搏：2.01 +/- 0.37 vs. 1.01 +/- 0.07 ml。min（-1）。g（-1），P < 0.05，VEGF vs.对照组）。在VEGF治疗的动物中观察到的局部冠状动脉血流的改善导致VEGF治疗的动物在起搏期间比对照动物更好地保持了内皮依赖性微血管舒张以及LCX区域中的LV缩短分数（对照组：7.1 +/- 2.6 vs. 3.6 +/-2.0%，静息vs.起搏; VEGF：6.9 +/- 2.9 vs. 6.3 +/-2.9%，静息vs.起搏）。我们的结论是，血管内皮生长因子管理在一个渐进的冠状动脉闭塞模型在猪冠状动脉血流改善和保存受损心肌的局部血流动力学。
Vascular endothelial growth factor (VEGF) is a potent mitogen capable of stimulating angiogenesis. We examined the effect of VEGF administration in a model of chronic porcine myocardial ischemia. Nineteen pigs were instrumented with proximal left circumflex coronary artery (LCX) Ameroid constrictors. in eight animals VEGF (2 mu g) with heparin (50 U) was administered extraluminally to the LCX myocardium with an osmotic pump for 4 wk and 11 other animals served as controls. VEGF-treated animals demonstrated higher flow in the LCX territory during both rest and pacing compared with untreated controls (rest: 1.35 +/- 0.1 vs. 0.80 +/- 0.09 ml . min(-1). g(-1); pacing: 2.01 +/- 0.37 vs. 1.01 +/- 0.07 ml . min(-1). g(-1), P < 0.05, VEGF vs. controls). The observed improvement in regional coronary flow in VEGF-treated animals resulted in better preservation of endothelium-dependent microvessel relaxation as well as fractional LV shortening in the LCX territory during pacing in the VEGF-treated than in control animals (controls: 7.1 +/- 2.6 vs. 3.6 +/- 2.0%, rest vs. pacing; VEGF: 6.9 +/- 2.9 vs. 6.3 +/- 2.9%, rest vs. pacing). We conclude that VEGF administration in a gradual coronary occlusion model in pigs results in improvement of coronary flow and preservation of regional hemodynamics in the compromised myocardium.