H-Wave® induces arteriolar vasodilation in rat striated muscle via nitric oxide-mediated mechanisms

• Published in: Journal of orthopaedic research Vol. 27; no. 9; pp. 1248 - 1251
• Main Authors: Smith, Thomas L., Blum, Kenneth, Callahan, Michael F., DiNubile, Nicholas A., Chen, Thomas J.H., Waite, Roger L.
• Format: Journal Article
• Language: English
• Published: Hoboken Wiley Subscription Services, Inc., A Wiley Company 01.09.2009
• Subjects: Animals; Arterioles - physiology; Electric Stimulation Therapy - instrumentation; Electric Stimulation Therapy - methods; Enzyme Inhibitors - pharmacology; H-Wave device; Male; microcirculation; Microcirculation - physiology; Muscle, Striated - blood supply; NG-Nitroarginine Methyl Ester - pharmacology; Nitric Oxide - metabolism; nitric oxide production; Rats; Rats, Sprague-Dawley; Regional Blood Flow - physiology; Soft Tissue Injuries - therapy; vascular mechanisms; Vasodilation - drug effects; Vasodilation - physiology
• ISSN: 0736-0266; 1554-527X
• DOI: 10.1002/jor.20851

H‐Wave® electrical device stimulation (HWDS) is used clinically to expedite recovery from soft tissue injuries. We hypothesized that HWDS induces arteriolar dilation, a mechanism involved in the healing process. Acute effects of HWDS on striated muscle arteriolar diameters were studied. Arteriolar diameters were measured in the cremaster muscle of 57 male anesthetized rats using intravital microscopy before and after HWDS or sham stimulation (SS) at 1 or 2 Hz for periods of 30–60 min. In a separate cohort, the role of nitric oxide (NO) in the response to HWDS was assessed by blocking NO synthase using topical L‐NAME at 10−5 M. Maximal arteriolar responses to stimulation were compared to prestimulation diameters. HWDS both at 1 and 2 Hz resulted in significant arteriolar vasodilation (p < 0.05). The arterioles in SS animals demonstrated no changes in diameter. Similarly, microvascular diameters did not change with HWDS following blockade of NO production. Because of Poiseuille's Law, the significant arteriolar dilation induced by HWDS would translate into increases in blood flow of 26–62%. In addition, lack of arteriolar dilation following HWDS with blockade of NO production suggests that NO plays a role in the microvascular response to HWDS. These studies suggest that arteriolar vasodilation accompanying HWDS may result in increased perfusion, contributing to the observed therapeutic effects of HWDS. © 2009 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res