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  • Title: Chronic low-dose aspirin therapy attenuates reflex cutaneous vasodilation in middle-aged humans.
    Author: Holowatz LA, Kenney WL.
    Journal: J Appl Physiol (1985); 2009 Feb; 106(2):500-5. PubMed ID: 19036898.
    Abstract:
    Full expression of reflex cutaneous vasodilation is dependent on cyclooxygenase- (COX) and nitric oxide synthase- (NOS) dependent mechanisms. Low-dose aspirin therapy is widely prescribed to inhibit COX-1 in platelets for atherothrombotic prevention. We hypothesized that chronic COX inhibition with daily low-dose aspirin therapy (81 mg) would attenuate reflex vasodilation in healthy human skin. Two microdialysis fibers were placed in forearm skin of seven middle-aged (57 +/- 3 yr), normotensive, healthy humans with no preexisting cardiovascular disease, taking daily low-dose aspirin therapy (aspirin: 81 mg), and seven unmedicated, healthy, age-matched control (no aspirin, 55 +/- 3 yr) subjects, with one site serving as a control (Ringer) and the other NOS inhibited (NOS inhibited: 10 mM N(G)-nitro-l-arginine methyl ester). Red cell flux was measured over each site by laser-Doppler flowmetry, as reflex vasodilation was induced by increasing core temperature (oral temperature) 1.0 degrees C using a water-perfused suit. Cutaneous vascular conductance (CVC) was calculated (CVC = flux/mean arterial pressure) and normalized to maximal CVC (CVC(max); 28 mM sodium nitroprusside). CVC(max) was not affected by either aspirin or NOS inhibition. The plateau in cutaneous vasodilation during heating (change in oral temperature = 1.0 degrees C) was significantly attenuated in the aspirin group (aspirin: 25 +/- 3% CVC(max) vs. no aspirin: 50 +/- 7% CVC(max), P < 0.001 between groups). NOS inhibition significantly attenuated %CVC(max) in both groups (aspirin: 17 +/- 2% CVC(max), no aspirin: 23 +/- 3% CVC(max); P < 0.001 vs. control), but this attenuation was less in the no-aspirin treatment group (P < 0.001). This is the first observation that chronic low-dose aspirin therapy attenuates reflex cutaneous vasodilation through both COX- and NOS-dependent mechanisms.
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