Hindlimb claudication reflects impaired nitric oxide-dependent revascularization after ischemia. [electronic resource]
Producer: 20070402Description: 10-5 p. digitalISSN:- 1537-1891
- Animals
- Arterial Occlusive Diseases -- complications
- Biomechanical Phenomena
- Blood Flow Velocity -- drug effects
- Disease Models, Animal
- Enzyme Induction
- Enzyme Inhibitors -- pharmacology
- Gait -- drug effects
- Hindlimb
- Intermittent Claudication -- etiology
- Ischemia -- etiology
- Locomotion -- drug effects
- Male
- Muscle, Skeletal -- blood supply
- NG-Nitroarginine Methyl Ester -- pharmacology
- Neovascularization, Physiologic
- Nitric Oxide -- metabolism
- Nitric Oxide Synthase Type III -- antagonists & inhibitors
- Peripheral Vascular Diseases -- complications
- RNA, Messenger -- biosynthesis
- Rats
- Rats, Wistar
- Recovery of Function
- Time Factors
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Publication Type: Journal Article; Research Support, Non-U.S. Gov't
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