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J Appl Physiol (April 11, 2003). doi:10.1152/japplphysiol.00254.2003
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Submitted on March 12, 2003
Accepted on April 6, 2003

Nitric Oxide Synthase Inhibition Does Not Alter the Reactive Hyperemic Response in the Cutaneous Circulation

Brett J Wong1, Brad W Wilkins1, Lacy A Holowatz1, and Christopher T Minson1*

1 Department of Exercise and Movement Science, University of Oregon, Eugene, OR, USA

* To whom correspondence should be addressed. E-mail: minson{at}oregon.uoregon.edu.

Reactive hyperemia is the sudden rise in blood flow following release of an arterial occlusion. Currently, the mechanisms mediating this response in the cutaneous circulation are poorly understood. The purpose of this study was to 1) characterize the reactive hyperemic response in the cutaneous circulation and 2) determine the contribution of NO to reactive hyperemia. Using laser-Doppler flowmetry, we characterized reactive hyperemia following 3-, 5-, 10-, and 15- minute arterial occlusions in ten subjects. The total hyperemic response was calculated by taking the area under the curve (AUC) of the hyperemic response minus baseline skin blood flow (SkBF) (i.e., total hyperemic response = AUC - [baseline SkBF x duration of hyperemic response in seconds]). For the characterization protocol, the total hyperemic response significantly increased as the period of ischemia increased from 5- to 15-minutes (P<0.05). However, the 3-minute response was not significantly different from the 5-minute response. In the NO-contribution protocol, two microdialysis fibers were placed in the forearm skin of 8 subjects. One site served as a control and was continuously perfused with Ringer's solution. The second site was continuously perfused with 10mM L-NAME to inhibit NO-synthase. Cutaneous vascular conductance (CVC) was calculated as flux/mean arterial pressure and normalized to maximal blood flow (28mM SNP). The total hyperemic response in control sites was not significantly different from L-NAME sites following a 5-minute occlusion (3261±890 vs. 2907±531 %CVCmax . sec). Similarly, total hyperemic responses in control sites were not different than L-NAME sites (9155±1121 vs. 9126±1088 %CVCmax . sec) following a 15-minute arterial occlusion. These data suggest NO does not directly mediate reactive hyperemia and NO is not produced in response to an increase in shear stress in the cutaneous circulation.




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