Collateral development and angiogenesis after major artery ligation does not alter hindquarter vascular reactivity in...

We tested whether vasodilator and vasoconstrictor responses of the hindquarter vasculature in conscious rabbits were altered 1 day, 2 weeks, and 6 months after bilateral superficial femoral artery ligation (SFAL). With pharmacological autonomic blockade, hindquarter flow (Doppler flowmeter) was restored to 84% of control values 1 day postligation (n = 5). Responses to aortic balloon inflation (5-80 s), and intraaortic infusion of norepinephrine, angiotensin II, serotonin, acetylcholine, sodium nitroprusside, and adenosine were similar to pre-SFAL responses. Two weeks post-SFAL, acrylic casts showed an extensive collateral network originating from branches of internal iliac and deep femoral arteries. Acetylcholine-induced dilatation was attenuated postligation (n = 7) relative to controls (n = 13). Serotonin caused constriction in two rabbits postligation but dilatation in all others; however responses to all other agents tested were similar to controls. Reactive hyperemia and vascular reactivity were similar in rabbits 6 months post-SFAL (n = 5) and controls (n = 5). Thus, despite extensive vascular remodeling after SFAL, global hyperemic flow responses of the rabbit hindquarter vasculature appeared normal. We found only minimal changes in vascular reactivity to constrictor and dilator stimuli. This model of peripheral vascular disease does not reflect the clinical syndrome.