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Basic fibroblast growth factor increases collateral blood flow in spontaneously hypertensive rats

¹Section of Vascular Surgery, University of Michigan, Ann Arbor, Michigan 48109; and ²Department of Biomedical Sciences, College of Veterinary Medicine, ³Department of Medical Pharmacology and Physiology, College of Medicine, and ⁴Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri 65211

Submitted 27 March 2003 ; accepted in final form 16 May 2003

Ischemia-induced angiogenic response is reduced in spontaneously hypertensive rats (SHR). To study whether exogenous basic fibroblast growth factor (bFGF) infusion is effective in expanding collateral circulation in frankly hypertensive SHR, femoral arteries of male SHR (weighing 250 g) were kept intact (nonoccluded control; n = 9) or occluded for4h(n = 12) or for 16 days with vehicle (n = 14) or bFGF [0.5 (n = 17), 5.0 (n = 13), and 50.0 (n = 14) µg · kg^–1 · day^–1 for 14 days] intraarterially. Maximal collateral-dependent blood flows (BF) to the hindlimbs were determined with ⁸⁵Sr- and ¹⁴¹Ce-labeled microspheres during running at 20 and 25 m/min (15% grade). Preexercise heart rates (530 beats/min) and blood pressures (BP; 200 mmHg) were similar across groups except in the high-dose bFGF group, where BP was reduced by 12% (P < 0.05). Femoral artery occlusion for 4 h resulted in 95% reduction of BF in calf muscles [199 ± 18.7 (nonoccluded group) to 10 ± 1.0 ml · min^–1 · 100 g^–1; P < 0.001]. BF to calf muscles of the vehicle and low-dose bFGF (0.5 µg · kg^–1 · day^–1) groups increased to 36 ± 3.2 and 45 ± 2.0 ml · min^–1 · 100 g^–1, respectively (P < 0.001). bFGF infusion at 5.0 and 50.0 µg · kg^–1 · day^–1 further increased (P < 0.001) BF to calf muscles (62 ± 4.6 and 62 ± 2.2 ml · min^–1 · 100 g^–1, respectively). Our results show that bFGF can effectively increase BF in hypertensive rats. The reduced hypertension with high-dose bFGF suggests that a critical signal in arteriogenesis (nitric oxide bioavailability) may be restored. These findings suggest that the dulled endothelial nitric oxide synthase of SHR does not preempt collateral vessel remodeling.

angiogenesis; vascular remodeling; peripheral arterial insufficiency; nitric oxide; arterial occlusion

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