Time course of increased cellular proliferation in collateral arteries after administration of vascular endothelial growth factor in a rabbit model of lower limb vascular insufficiency.

摘要: Proliferation of vascular cells has been previously shown to contribute spontaneous development coronary collaterals. Recent studies from several laboratories have established that collateral artery growth in both the heart and limb can be enhanced by administration angiogenic factors, or therapeutic angiogenesis. In this study, we sought (1) define extent time course endothelial cell (EC) smooth muscle (SMC) proliferation accompanying during ischemia (2) determine which proliferative activity ECs SMCs is augmented angiogenesis with factor (VEGF), a heparin-binding EC-specific mitogen. Ten days after induction surgically excising femoral rabbits, either VEGF (500 1000 micrograms) saline was administered as bolus into iliac ischemic limb. Cellular evaluated bromodeoxyuridine labeling for 24 hours at day 0 (immediately before administration) 3, 5, 7 VEGF, EC midzone collaterals VEGF-treated animals increased 2.8-fold 5 (P < 0.05 versus control), returned baseline levels 7. SMC also 2.7-fold response 0.05). No significant increase observed stem re-entry compared untreated control animals. Reduction hemodynamic deficit measured lower blood pressure documented 0.01 untreated, control). These data thus establish contribution cellular vessel support concept contributes formation vessels VEGF.