Therapeutic aspirin therapy attenuates reflex cutaneous vasodilation in middle‐aged human skin

Abstract

Full expression of reflex cutaneous vasodilation (VD) is dependent on cyclooxygenase‐ (COX) and nitric oxide synthase‐ (NOS) dependent mechanisms. Low‐dose therapeutic aspirin (ASA) therapy is utilized clinically in healthy populations to inhibit platelet aggregation for stroke prevention, however chronic COX inhibition may attenuate COX‐dependent VD mechanisms. We hypothesized that chronic COX inhibition with daily low‐dose ASA therapy would attenuated reflex VD in healthy humans. Two microdialysis (MD) fibers were placed in forearm skin of 4 middle‐aged (ASA: 57±3 years) normotensive humans taking daily low‐dose ASA therapy (81mg) and 4 unmedicated age‐matched control (no ASA: 56±2 years) subjects to serve as control (C: Ringers) and NOS inhibited (NOS‐I: 10mM L‐NAME) sites. VD was induced by using a water‐perfused suit to increase core temperature 0.8°C. Red cell flux was measured by laser‐Doppler over each site. Cutaneous vascular conductance was calculated (CVC=flux/MAP) and normalized to maximal CVC (28mM SNP). Cutaneous VD during heating was attenuated with daily low‐dose ASA treatment (ASA: 19±3 vs. no ASA: 49±5%CVCmax, p<0.01). NOS‐I decreased CVC in the no ASA group (21±4%CVCmax; p<0.05 vs. C), but failed to decrease CVC in the daily ASA treatment group (13±4%CVCmax). Daily low‐dose ASA therapy attenuates reflex cutaneous VD in middle‐aged humans though COX‐ and NOS‐dependent VD mechanisms.