Abstract
Individuals of African descent (AFD) are more susceptible to non-freezing cold injury (NFCI) than Caucasians (CAU) [1]. This may be a consequence of lower skin blood flow during local cold exposure and subsequent rewarming in AFD [2], possibly due to a difference in endothelium function as acetylcholine (ACh)-induced vasodilatation is smaller in AFD than CAU on the non-glabrous finger and toe skin sites [3]. It is known that prostaglandins produced by the enzyme cyclooxygenase (COX) mediate part of the ACh-induced vasodilator response [4] however in hypertensive individuals, COX inhibition results in augmented vasodilatation in response to ACh [5] demonstrating that COX can also promote vasoconstriction. Whether COX products are involved in the attenuated vasodilator response to ACh in healthy AFD [3] is not known. Therefore, the aim of the present study was to investigate the contribution of COX in both CAU and AFD to local application of ACh in foot and finger skin sites which are susceptible to NFCI.
Highlights
Individuals of African descent (AFD) are more susceptible to non-freezing cold injury (NFCI) than Caucasians (CAU) [1]
Foot: ACh elicited a greater vasodilatation in CAU than AFD following placebo (Median [interquartile], CAU n = 12, AFD n = 12, max%Δ: 943[490] % vs 81[370] %, P = 0.003; area under the curve (AUC): 4516[2601] vs 190[1329], P = 0.001) and aspirin (Median [interquartile], max%Δ: 775[784] % vs 50[148] %, P < 0.000; AUC: 3120[3170] vs 95[894], P = 0.002)
Aspirin reduced the response to ACh in CAU only (AUC P = 0.031)
Summary
Individuals of African descent (AFD) are more susceptible to non-freezing cold injury (NFCI) than Caucasians (CAU) [1]. This may be a consequence of lower skin blood flow during local cold exposure and subsequent rewarming in AFD [2], possibly due to a difference in endothelium function as acetylcholine (ACh)-induced vasodilatation is smaller in AFD than CAU on the nonglabrous finger and toe skin sites [3].
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