Homeostatic Responses to Subsystolic Arterial Occlusive Pressure in Glabrous and Non-Glabrous Skin Circulation

Background: Reactive hyperemia (RH) is used to assess microcirculatory function in vivo and has traditionally been interpreted as a local, ischemia-driven vasodilatory response following arterial occlusion. However, perfusion changes consistently observed in contralateral, non-challenged limbs question the exclusively local nature of RH. Objective: This study aimed to characterize reactive hyperemic responses elicited by subsystolic cuff pressures, below arterial occlusion pressure (AOP), and to investigate their effects on glabrous and non-glabrous skin microcirculation and on global hemodynamics. Methods: Seven healthy women underwent a standardized protocol consisting of baseline stabilization, a 2 min subsystolic cuff inflation (70-80% of resting AOP) in one arm, and a recovery period. Microvascular perfusion was simultaneously assessed in both hands using laser Doppler flowmetry (LDF) on glabrous skin and polarized light spectroscopy (PSp) on non-glabrous dorsal skin. Hemodynamic indicators were continuously monitored using CNAP (Continuous Non-invasive Arterial Pressure) technology. Ipsilateral and contralateral responses were compared across experimental phases. Results: Subsystolic cuff inflation induced significant perfusion changes not only in the challenged limb but also in the contralateral limb, despite the absence of a complete arterial occlusion. Conclusions: These findings confirm the adaptive nature of RH emphasizing the major role for the sympathetic nervous system in glabrous skin. In glabrous (palmar) skin, a similar perfusion profile is shown in both hands but significant differences could only be found in the ipsilateral hand. In contrast, non-glabrous (dorsal) skin demonstrated region-specific increases in perfusion, again evident in the ipsilateral hand, suggesting venous stasis. No changes in global hemodynamic variables were observed throughout the protocol. Further studies in larger, more diverse populations are needed to confirm these observations and refine the mechanistic understanding of reactive hyperemia.