Gregory W McGarr1, Gary J Hodges1, Matthew M Mallette1, Stephen S Cheung2. 1. Environmental Ergonomics Laboratory, Department of Kinesiology, Brock University, St. Catharines, ON L2S 3A1, Canada. 2. Environmental Ergonomics Laboratory, Department of Kinesiology, Brock University, St. Catharines, ON L2S 3A1, Canada. Electronic address: scheung@brocku.ca.
Abstract
BACKGROUND: Ischemia-reperfusion (IR) injury impairs microcirculatory function by reducing nitric oxide (NO) bioavailability and increasing sympathetic tone. This study non-invasively examined the effects of acute upper limb IR injury on local thermal hyperemia (LTH) in glabrous and non-glabrous finger skin. MATERIALS AND METHODS: In ten healthy males, LTH was examined twice (~7-10 d apart) for each skin type on the index finger using laser-Doppler flowmetry in a counterbalanced design with either 1) 20 min ischemia, followed by reperfusion (ISCH) or 2) time-matched control (SHAM). LTH tests were performed using a standard heating protocol (33-42 °C at 1 °C·20 s-1 + 20 min at 44 °C) and baseline, initial peak, nadir, delayed plateau and maximal heating phases were identified as well as vasodilatory onset time and time to initial peak. Cutaneous vasomotion was evaluated using spectral analysis and comparing absolute and normalized wavelet amplitudes between conditions for both skin types at baseline and during LTH. RESULTS: In non-glabrous skin, IR injury delayed the vasodilatory onset of local heating by 27.4 [11.3, 43.4] s (p = 0.004) and attenuated cutaneous vasodilation during the initial peak and sustained heating by -44.5 [-73.0, -15.9] PU (p = 0.003) and -34.4 [-62.9, -5.8] PU (p = 0.020), respectively. Analysis of normalized wavelet amplitudes in non-glabrous skin identified impaired microvascular function at baseline via NO-dependent mechanisms (-3.64 [-7.22, -0.05] %, p = 0.047), and during LTH via respiratory influences (-2.83 [-5.39, -0.21] %, p = 0.031). In glabrous skin, IR injury delayed vasodilatory onset time by 24.9 [1.1, 67.6] s (p = 0.042). The vasodilatory response to sustained local skin heating in glabrous skin was increased following IR injury (+56.3 [15.1, 116.5], p = 0.012), however, this was not evident when accounting for differences in blood pressure between conditions. Additionally, no other differences in vasodilatory or vasomotor functions were observed in this skin type between conditions (all, p > 0.05). CONCLUSIONS: The current IR model elicits impaired cutaneous vasodilatory responses to local heating in young males, primarily in non-glabrous skin, and may be useful for exploring mechanisms of IR-injury and for testing potential countermeasures in otherwise healthy humans.
BACKGROUND:Ischemia-reperfusion (IR) injury impairs microcirculatory function by reducing nitric oxide (NO) bioavailability and increasing sympathetic tone. This study non-invasively examined the effects of acute upper limb IR injury on local thermal hyperemia (LTH) in glabrous and non-glabrous finger skin. MATERIALS AND METHODS: In ten healthy males, LTH was examined twice (~7-10 d apart) for each skin type on the index finger using laser-Doppler flowmetry in a counterbalanced design with either 1) 20 min ischemia, followed by reperfusion (ISCH) or 2) time-matched control (SHAM). LTH tests were performed using a standard heating protocol (33-42 °C at 1 °C·20 s-1 + 20 min at 44 °C) and baseline, initial peak, nadir, delayed plateau and maximal heating phases were identified as well as vasodilatory onset time and time to initial peak. Cutaneous vasomotion was evaluated using spectral analysis and comparing absolute and normalized wavelet amplitudes between conditions for both skin types at baseline and during LTH. RESULTS: In non-glabrous skin, IR injury delayed the vasodilatory onset of local heating by 27.4 [11.3, 43.4] s (p = 0.004) and attenuated cutaneous vasodilation during the initial peak and sustained heating by -44.5 [-73.0, -15.9] PU (p = 0.003) and -34.4 [-62.9, -5.8] PU (p = 0.020), respectively. Analysis of normalized wavelet amplitudes in non-glabrous skin identified impaired microvascular function at baseline via NO-dependent mechanisms (-3.64 [-7.22, -0.05] %, p = 0.047), and during LTH via respiratory influences (-2.83 [-5.39, -0.21] %, p = 0.031). In glabrous skin, IR injury delayed vasodilatory onset time by 24.9 [1.1, 67.6] s (p = 0.042). The vasodilatory response to sustained local skin heating in glabrous skin was increased following IR injury (+56.3 [15.1, 116.5], p = 0.012), however, this was not evident when accounting for differences in blood pressure between conditions. Additionally, no other differences in vasodilatory or vasomotor functions were observed in this skin type between conditions (all, p > 0.05). CONCLUSIONS: The current IR model elicits impaired cutaneous vasodilatory responses to local heating in young males, primarily in non-glabrous skin, and may be useful for exploring mechanisms of IR-injury and for testing potential countermeasures in otherwise healthy humans.
Authors: Joel T Greenshields; Jason M Keeler; Jessica A Freemas; Tyler B Baker; Blair D Johnson; Stephen J Carter; Zachary J Schlader Journal: Physiol Rep Date: 2021-10
Authors: Sophie Lalande; Holden W Hemingway; Caitlin P Jarrard; Amy M Moore; Albert H Olivencia-Yurvati; Rauchelle E Richey; Steven A Romero Journal: Am J Physiol Regul Integr Comp Physiol Date: 2021-07-14 Impact factor: 3.210