Local sensory nerve control of skin blood flow during local warming in type 2 diabetes mellitus

Abstract

SM, Charkoudian N. Local sensory nerve control of skin blood flow during local warming in type 2 diabetes mellitus. J Appl Physiol 108: 293-297, 2010. First published December 3, 2009 doi:10.1152/japplphysiol.01077.2009.-Cutaneous sensory nerve-mediated vasodilation is an important component of normal microvascular responsiveness to thermal and nonthermal stimuli. Since both neural and microvascular function can be impaired in type 2 diabetes mellitus (T2DM), we tested the hypothesis that local sensory nerve-mediated vasodilation during nonpainful local warming of the skin is less in T2DM compared with healthy controls (C) matched for age and body size. The rapid vasodilation during the first ϳ5 min of this local warming ("initial peak") was previously shown to rely primarily on local sensory nerves. We measured skin blood flow in T2DM and C subjects (n ϭ 7 in each group) at baseline and during 35 min of local warming of the skin to 42°C at two sites on the ventral forearm. One site was pretreated with 4% lidocaine (LIDO) to block local sensory innervation. During local warming, cutaneous vascular conductance (CVC) during the initial peak was not different between groups, either at the untreated site [T2DM 75 Ϯ 2 vs. C 81 Ϯ 6% of maximum CVC (%maxCVC); P Ͼ 0.05] or at the LIDO site (T2DM 63 Ϯ 7 vs. C 64 Ϯ 6%maxCVC; P Ͼ 0.05). The difference between untreated and LIDO sites (sensory nerve contribution) was also similar between groups (T2DM 13 Ϯ 5 vs. C 18 Ϯ 5%maxCVC; P Ͼ 0.05) and was smaller with LIDO than was previously shown with other local anesthetics. Our results suggest that relatively healthy individuals with T2DM do not exhibit impairments in local sensory nerve vasodilation during thermal stimulation compared with controls of similar age and body size. cutaneous circulation; vasodilation; temperature; metabolic syndrome IN HUMANS, nonpainful local warming of the skin elicits a biphasic vasodilation involving local sensory nerve mechanisms and nitric oxide (6, 8). Initial, rapid blood flow increases during the first 3-5 min (called the "initial peak" of the vasodilator response) are thought to be caused primarily by direct action of local sensory nerves, potentially through release of local vasodilators such as calcitonin gene-related peptide (CGRP) and substance P (5, 8). The second phase of the vasodilation is nitric oxide dependent and occurs over a longer period, typically 25-30 min, after which a plateau in blood flow is reached (6,8).Type 2 diabetes mellitus (T2DM) is strongly associated with neural and microvascular dysfunction. As the incidence and prevalence of T2DM are increasing, also increasing are the number of individuals who are otherwise relatively healthy and live with T2DM but manage it well so that the number of comorbid conditions is minimal. We have therefore focused our efforts on this growing population in our attempts to understand mechanisms of cutaneous microvascular dysfunction in T2DM (12)(13)(14). Recent studies in our laboratory have shown that relatively healthy individual...

The contribution of sensory nerves to cutaneous vasodilatation of the forearm and leg to local skin heating

“…This finding is congruent with others who have investigated sensory nerve involvement in the hyperemic response to a local heating stimulus in the forearm (Carter and Hodges 2011;Tew et al 2011a;Strom et al 2010;Minson et al 2001) as well as with those using whole body heating (Wong 2013;Hodges et al 2009). These data suggest that cutaneous sensory nerves play little, if any role in the sustained vasodilatation to local heating of the skin of either the forearm or the leg.…”

The contribution of sensory nerves to the onset threshold for cutaneous vasodilatation during gradual local skin heating of the forearm and leg

“…Localized heating of the skin elicits a biphasic vasodilatory response. There is an early, rapid vasodilatation during the first 5 min of heating ('initial peak') that is dependent on local sensory nerve function (Carter and Hodges, 2011;Hodges et al, 2015;Minson et al, 2001;Strom et al, 2010;Tew et al, 2011). This is succeeded by a secondary, gradual and prolonged vasodilatation (plateau phase) that is dependent on endothelial nitric oxide (eNOS) (Hodges and Sparks, 2013;Kellogg et al, 2008Kellogg et al, , 2009 and endothelial derived hyperpolarizing factor (Brunt and Minson, 2012).…”

Do Heat Events Pose a Greater Health Risk for Individuals with Type 2 Diabetes?

“…For a comprehensive overview of these mechanisms, the reader is referred to the review by Kenny and Journeay. 4 Although only one study to date has examined whole-body heat loss in individuals with type 2 diabetes, 5 several studies have examined the local heat loss responses of SkBF [6][7][8][9][10][11][12][13][14][15] and sweating. [16][17][18][19] Many of these studies found impairments in local heat loss responses in individuals with type 2 diabetes compared with matched controls.…”