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

Abstract

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.