Role of cyclooxygenase in the vascular responses to extremity cooling in Caucasian and African descent males

Compared with Caucasians (CAU), African descent (AFD) individuals are more susceptible to non-freezing cold injury (NFCI) (DeGroot et al., 2003), perhaps due to experiencing greater cutaneous vasoconstriction and cooler finger skin temperatures during extremity cooling (Maley et al., 2014). Given that AFD have greater levels of oxidative stress, perhaps produced through the enzyme cyclooxygenase (COX) (Vanhoutte, 2011), and that COX produces the vasoconstrictor thromboxane A₂, it is possible that this enzyme may contribute to the accentuated vasoconstrictor response in AFD during local cooling.

Using a placebo-controlled, crossover design the present study tested the hypothesis that COX may, in part, be responsible for the exaggerated vasoconstrictor response to local cooling in AFD. Twelve AFD and twelve CAU young healthy males completed foot cooling and hand cooling (separately, in 8 °C water for 30 minutes, hand / foot in a plastic bag during immersion) with spontaneous rewarming in 30 °C air following placebo or aspirin (COX inhibition) treatment. Skin blood flow, expressed as cutaneous vascular conductance (flux•mmHg^-1), and skin temperature (T_sk) were measured throughout.

Toe skin blood flow and T_sk did not differ between ethnicities during foot cooling. However, responses to hand cooling differed between ethnicities. Responses to both foot and hand cooling principally did not differ between placebo and COX inhibition. Specifically, during hand cooling following placebo, AFD experienced a lower minimum finger skin blood flow (0.5 [0.1] vs.0.8 [0.2] flux•mmHg^-1, P< 0.001) and a lower minimum finger T_sk (9.5 [1.4] °C vs. 10.7 [1.3] °C, P= 0.039) compared with CAU. During spontaneous rewarming average skin blood flow was also lower in AFD than CAU (2.8 [1.6] vs.4.3 [1.0] flux•mmHg^-1, P< 0.001).

These data provide further support that AFD experience an exaggerated response to hand cooling; however, the results demonstrate the COX pathway is not the primary reason for the exaggerated responses in AFD and increased susceptibility to NFCI.