Prostanoids contribute to cutaneous active vasodilation in humans

Area of Science:

• Physiology
• Thermoregulation
• Cardiovascular Research

Background:

• Cutaneous active vasodilation mechanisms during heat stress are not fully understood.
• The role of the cyclooxygenase (COX) pathway in this process requires further investigation.

Purpose of the Study:

• To determine if the COX pathway contributes to active vasodilation during whole body heat stress.
• To verify if the COX pathway influences the cutaneous hyperemic response during local heating.

Main Methods:

• Microdialysis fibers infused with Ringer, ketorolac (COX inhibitor), L-NAME (nitric oxide synthase inhibitor), or combined inhibitors in forearm skin.
• Whole body heating and local heating protocols to induce vasodilation and hyperemia.
• Laser-Doppler flowmetry measured red blood cell flux (RBC flux) and calculated cutaneous vascular conductance (CVC).

Main Results:

• During whole body heating, CVC was significantly reduced at ketorolac, L-NAME, and combined inhibitor sites compared to control.
• The combined ketorolac and L-NAME site showed significantly lower CVC than sites with single inhibitors.
• Local heating response did not differ between control and ketorolac sites, or between L-NAME and combined inhibitor sites.

Conclusions:

• Prostanoids, mediated by the COX pathway, contribute to active vasodilation during whole body heat stress.
• The COX pathway does not play a significant role in the cutaneous hyperemic response to local heating.