1. Nitrite anion stimulates ischemic arteriogenesis involving NO metabolism.
- Author
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Bir SC, Pattillo CB, Pardue S, Kolluru GK, Docherty J, Goyette D, Dvorsky P, and Kevil CG
- Subjects
- Angiography, Animals, Chronic Disease, Collateral Circulation drug effects, Collateral Circulation physiology, Femoral Artery drug effects, Femoral Artery physiopathology, Femoral Artery surgery, Femoral Vein drug effects, Femoral Vein physiopathology, Femoral Vein surgery, Hindlimb blood supply, Hindlimb drug effects, Hindlimb physiopathology, Ischemia drug therapy, Ischemia physiopathology, Mice, Mice, Inbred C57BL, Regional Blood Flow drug effects, Regional Blood Flow physiology, Severity of Illness Index, Neovascularization, Physiologic drug effects, Nitric Oxide metabolism, Nitric Oxide Donors administration & dosage, Prodrugs administration & dosage, Sodium Nitrite administration & dosage
- Abstract
Nitric oxide (NO) is a potential regulator of ischemic vascular remodeling, and as such therapies augmenting its bioavailability may be useful for the treatment of ischemic tissue diseases. Here we examine the effect of administering the NO prodrug sodium nitrite on arteriogenesis activity during established tissue ischemia. Chronic hindlimb ischemia was induced by permanent unilateral femoral artery and vein ligation. Five days postligation; animals were randomized to control PBS or sodium nitrite (165 μg/kg) therapy twice daily. In situ vascular remodeling was measured longitudinally using SPY angiography and Microfil vascular casting. Delayed sodium nitrite therapy rapidly increased ischemic limb arterial vessel diameter and branching in a NO-dependent manner. SPY imaging angiography over time showed that nitrite therapy enhanced ischemic gracillis collateral vessel formation from the profunda femoris to the saphenous artery. Immunofluorescent staining of smooth muscle cell actin also confirmed that sodium nitrite therapy increased arteriogenesis in a NO-dependent manner. The NO prodrug sodium nitrite significantly increases arteriogenesis and reperfusion of established severe chronic tissue ischemia.
- Published
- 2012
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