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J Appl Physiol 106: 500-505, 2009. First published November 26, 2008; doi:10.1152/japplphysiol.91215.2008
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Chronic low-dose aspirin therapy attenuates reflex cutaneous vasodilation in middle-aged humans

Lacy A. Holowatz1 and W. Larry Kenney1,2

Departments of 1Kinesiology and 2Graduate Physiology Program, Noll Laboratory, The Pennsylvania State University, University Park, Pennsylvania

Submitted 10 September 2008 ; accepted in final form 25 November 2008

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 NG-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°C using a water-perfused suit. Cutaneous vascular conductance (CVC) was calculated (CVC = flux/mean arterial pressure) and normalized to maximal CVC (CVCmax; 28 mM sodium nitroprusside). CVCmax was not affected by either aspirin or NOS inhibition. The plateau in cutaneous vasodilation during heating (change in oral temperature = 1.0°C) was significantly attenuated in the aspirin group (aspirin: 25 ± 3% CVCmax vs. no aspirin: 50 ± 7% CVCmax, P < 0.001 between groups). NOS inhibition significantly attenuated %CVCmax in both groups (aspirin: 17 ± 2% CVCmax, no aspirin: 23 ± 3% CVCmax; 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.

thermoregulation; prostaglandins; cyclooxygenase; nitric oxide



Address for reprint requests and other correspondence: L. A. Holowatz, 204 Noll Laboratory, Univ. Park, PA 16802 (e-mail: lma191{at}psu.edu)




This article has been cited by other articles:


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J. Appl. Physiol.Home page
G. Mahe, P. Rousseau, J. L. Saumet, and P. Abraham
About "Chronic low-dose aspirin therapy attenuates reflex cutaneous vasodilatation in middle-aged humans"
J Appl Physiol, April 1, 2009; 106(4): 1471 - 1471.
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J. Appl. Physiol.Home page
L. A. Holowatz and W. L. Kenney
Reply to Mahe, Rousseau, Saumet, and Abraham
J Appl Physiol, April 1, 2009; 106(4): 1472 - 1472.
[Full Text] [PDF]




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