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Am J Physiol Regul Integr Comp Physiol (February 16, 2006). doi:10.1152/ajpregu.00710.2005
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Submitted on October 4, 2005
Accepted on February 15, 2006

Prostanoids contribute to cutaneous active vasodilation in humans

Gregg R McCord1, Jean-Luc Cracowski2, and Christopher T Minson1*

1 Human Physiology, University of Oregon, Eugene, OR, USA
2 Human Physiology, University of Oregon, Eugene, OR, USA; HP2 Laboratory, Grenoble Medical School, Grenoble, France

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

The specific mechanisms by which skin blood flow increases in response to a rise in core body temperature via cutaneous active vasodilation is poorly understood. The primary purpose of this study was to determine whether the COX-pathway contributes to active vasodilation during whole body heat stress (protocol 1; n=9). A secondary goal was to verify that the COX-pathway does not contribute to the cutaneous hyperemic response during local heating (protocol 2; n=4). For both protocols, four microdialysis fibers were placed in forearm skin. Sites were randomly assigned and perfused with 1) Ringers solution (control-site), 2) Ketorolac (KETO), a COX-1/COX-2 pathway inhibitor, 3) NG-nitro-L-arginine methyl ester (L-NAME), a NO-synthase inhibitor, and 4) a combination of KETO and L-NAME. During the first protocol, active vasodilation was induced using whole body heating with water perfused suits. The second protocol used local heaters to induce a local hyperemic response. Red blood cell flux (RBC flux) was indexed at all sites using laser-Doppler flowmetry, and cutaneous vascular conductance (CVC; RBC flux/mean arterial pressure) was normalized to maximal vasodilation at each site. During whole body heating, CVC values at sites perfused with KETO (43±9%CVCmax), L-NAME (35±9%CVCmax), and combined KETO/L-NAME (22±8%CVCmax) were significantly decreased with respect to the control site (59±7%CVCmax) (P<0.05). Additionally, CVC at the combined KETO/L-NAME site was significantly decreased compared to sites infused with KETO or L-NAME alone (P<0.05). In the second protocol, the hyperemic response to local heating did not differ between the control site and KETO site or between the L-NAME and KETO/L-NAME site. These data suggest that prostanoids contribute to active vasodilation, but do not play a role during local thermal hyperemia.




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