Effect of sensory blockade and rate of sensory stimulation on local heating induced axon reflex response in facial skin

2021 ◽  
Vol 233 ◽  
pp. 102809
Author(s):  
Kristen Metzler-Wilson ◽  
Thad E. Wilson ◽  
Samantha M. Ausmus ◽  
Austin M. Sventeckis
2012 ◽  
Vol 84 (3) ◽  
pp. 356-361 ◽  
Author(s):  
Claire Millet ◽  
Matthieu Roustit ◽  
Sophie Blaise ◽  
Jean-Luc Cracowski

2006 ◽  
Vol 572 (3) ◽  
pp. 811-820 ◽  
Author(s):  
Belinda L. Houghton ◽  
Jessica R. Meendering ◽  
Brett J. Wong ◽  
Christopher T. Minson

2008 ◽  
Vol 105 (1) ◽  
pp. 233-240 ◽  
Author(s):  
Gary J. Hodges ◽  
Wojciech A. Kosiba ◽  
Kun Zhao ◽  
John M. Johnson

Presynaptic blockade of cutaneous vasoconstrictor nerves (VCN) abolishes the axon reflex (AR) during slow local heating (SLH) and reduces the vasodilator response. In a two-part study, forearm sites were instrumented with microdialysis fibers, local heaters, and laser-Doppler flow probes. Sites were locally heated from 33 to 40°C over 70 min. In part 1, we tested whether this effect of VCN acted via nitric oxide synthase (NOS). In five subjects, treatments were as follows: 1) untreated; 2) bretylium, preventing neurotransmitter release; 3) NG-nitro-l-arginine methyl ester (l-NAME) to inhibit NOS; and 4) combined bretylium + l-NAME. At treated sites, the AR was absent, and there was an attenuation of the ultimate vasodilation ( P < 0.05), which was not different among those sites ( P > 0.05). In part 2, we tested whether norepinephrine and/or neuropeptide Y is involved in the cutaneous vasodilator response to SLH. In seven subjects, treatments were as follows: 1) untreated; 2) propranolol and yohimbine to antagonize α- and β-receptors; 3) BIBP-3226 to antagonize Y1 receptors; and 4) combined propranolol + yohimbine + BIBP-3226. Treatment with propranolol + yohimbine or BIBP-3226 significantly increased the temperature at which AR occurred ( n = 4) or abolished it ( n = 3). The combination treatment consistently eliminated it. Importantly, ultimate vasodilation with SLH at the treated sites was significantly ( P < 0.05) less than at the control. These data suggest that norepinephrine and neuropeptide Y are important in the initiation of the AR and for achieving a complete vasodilator response. Since VCN and NOS blockade in combination do not have an inhibition greater than either alone, these data suggest that VCN promote heat-induced vasodilation via a nitric oxide-dependent mechanism.


2009 ◽  
Vol 106 (4) ◽  
pp. 1065-1071 ◽  
Author(s):  
Noortje T. L. Van Duijnhoven ◽  
Thomas W. J. Janssen ◽  
Daniel J. Green ◽  
Christopher T. Minson ◽  
Maria T. E. Hopman ◽  
...  

Spinal cord injury (SCI) induces vascular adaptations below the level of the lesion, such as impaired cutaneous vasodilation. However, the mechanisms underlying these differences are unclear. The aim of this study is to examine arm and leg cutaneous vascular conductance (CVC) responses to local heating in 17 able-bodied controls (39 ± 13 yr) and 18 SCI subjects (42 ± 8 yr). SCI subjects were counterbalanced for functional electrostimulation (FES) cycling exercise (SCI-EX, n = 9) or control (SCI-C, n = 9) and reanalyzed after 8 wk. Arm and leg skin blood flow were measured by laser-Doppler flowmetry during local heating (42°C), resulting in an axon-reflex mediated first peak, nadir, and a primarily nitric oxide-dependent plateau phase. Data were expressed as a percentage of maximal CVC (44°C). CVC responses to local heating in the paralyzed leg, but also in the forearm of SCI subjects, were lower than in able-bodied controls ( P < 0.05 and 0.01, respectively). The 8-wk intervention did not change forearm and leg CVC responses to local heating in SCI-C and SCI-EX, but increased femoral artery diameter in SCI-EX ( P < 0.05). Interestingly, findings in skin microvessels contrast with conduit arteries, where physical (in)activity contributes to adaptations in SCI. The lower CVC responses in the paralyzed legs might suggest a role for inactivity in SCI, but the presence of impaired CVC responses in the normally active forearm suggests other mechanisms. This is supported by a lack of adaptation in skin microcirculation after FES cycle training. This might relate to the less frequent and smaller magnitude of skin blood flow responses to heat stimuli, compared with controls, than physical inactivity per se.


1996 ◽  
Vol 271 (5) ◽  
pp. G876-G883 ◽  
Author(s):  
A. P. Gokin ◽  
L. J. Jennings ◽  
G. M. Mawe

The actions of calcitonin gene-related peptide (CGRP) have been determined from intracellular recordings obtained from gallbladder neurons in intact whole mount preparations. In most cells, pressure microejection of CGRP elicited a slow, monophasic depolarization, 4 mV in amplitude, that was associated with a decrease in input resistance and increased excitability. The CGRP-induced depolarization was attenuated in a low-Na+ solution and had a reversal potential of -8 mV. In 10% of the cells, microejection of CGRP elicited a biphasic response that was composed of a rapid transient depolarization followed by a slow depolarization that was similar to the monophasic response. Addition of CGRP (1–10 nM) to the bathing solution elicited a monophasic depolarization and desensitized the cells to applications of CGRP by microejection. Forskolin, applied either by microejection or bath application, also depolarized gallbladder neurons and produced cross-desensitization to CGRP. Responses to substance P were not enhanced by CGRP, and CGRP did not affect fast synaptic responses. It is concluded that CGRP may contribute to a local axon reflex response in gallbladder ganglia.


2015 ◽  
Vol 114 (3) ◽  
pp. 1530-1537 ◽  
Author(s):  
Kristen Metzler-Wilson ◽  
Kumika Toma ◽  
Dawn L. Sammons ◽  
Sarah Mann ◽  
Andrew J. Jurovcik ◽  
...  

Facial flushing in rosacea is often induced by trigger events. However, trigger causation mechanisms are currently unclear. This study tested the central hypothesis that rosacea causes sympathetic and axon reflex-mediated alterations resulting in trigger-induced symptomatology. Twenty rosacea patients and age/sex-matched controls participated in one or a combination of symptom triggering stressors. In protocol 1, forehead skin sympathetic nerve activity (SSNA; supraorbital microneurography) was measured during sympathoexcitatory mental (2-min serial subtraction of novel numbers) and physical (2-min isometric handgrip) stress. In protocol 2, forehead skin blood flow (laser-Doppler flowmetry) and transepithelial water loss/sweat rate (capacitance hygrometry) were measured during sympathoexcitatory heat stress (whole body heating by perfusing 50°C water through a tube-lined suit). In protocol 3, cheek, forehead, forearm, and palm skin blood flow were measured during nonpainful local heating to induce axon reflex vasodilation. Heart rate (HR) and mean arterial pressure (MAP) were recorded via finger photoplethysmography to calculate cutaneous vascular conductance (CVC; flux·100/MAP). Higher patient transepithelial water loss was observed (rosacea 0.20 ± 0.02 vs. control 0.10 ± 0.01 mg·cm−2·min−1, P < 0.05). HR and MAP changes were not different between groups during sympathoexcitatory stressors or local heating. SSNA during early mental (32 ± 9 and 9 ± 4% increase) and physical (25 ± 4 and 5 ± 1% increase, rosacea and controls, respectively) stress was augmented in rosacea (both P < 0.05). Heat stress induced more rapid sweating and cutaneous vasodilation onset in rosacea compared with controls. No axon reflex vasodilation differences were observed between groups. These data indicate that rosacea affects SSNA and that hyperresponsiveness to trigger events appears to have a sympathetic component.


2002 ◽  
Vol 93 (5) ◽  
pp. 1644-1649 ◽  
Author(s):  
Christopher T. Minson ◽  
Lacy A. Holowatz ◽  
Brett J. Wong ◽  
W. Larry Kenney ◽  
Brad W. Wilkins

Cutaneous vasodilation is reduced in healthy older vs. young subjects; however, the mechanisms that underlie these age-related changes are unclear. Our goal in the present study was to determine the role of nitric oxide (NO) and the axon reflexes in the skin blood flow (SkBF) response to local heating with advanced age. We placed two microdialysis fibers in the forearm skin of 10 young (Y; 22 ± 2 yr) and 10 older (O; 77 ± 5 yr) men and women. SkBF over each site was measured by laser-Doppler flowmetry (LDF; Moor DRT4). Both sites were heated to 42°C for ∼60 min while 10 mM N G-nitro-l-arginine methyl ester (l-NAME) was infused throughout the protocol to inhibit NO synthase (NOS) in one site and 10 mM l-NAME was infused after 40 min of local heating in the second site. Data were expressed as a percentage of maximal vasodilation (%CVCmax; 28 mM nitroprusside infusion). Local heating beforel-NAME infusion resulted in a significantly reduced initial peak (Y: 61 ± 2%CVCmax vs. O: 46 ± 4%CVCmax) and plateau (Y: 93 ± 2%CVCmaxvs. O: 82 ± 5%CVCmax) CVC values in older subjects ( P < 0.05). When NOS was inhibited after 40 min of heating, CVC declined to the same value in the young and older groups. Thus the overall contribution of NO to the plateau phase of the SkBF response to local heating was less in the older subjects. The initial peak response was significantly lower in the older subjects in both microdialysis sites (Y: 52 ± 4%CVCmax vs. O: 38 ± 5%CVCmax; P < 0.05). These data suggest that age-related changes in both axon reflex-mediated and NO-mediated vasodilation contribute to attenuated cutaneous vasodilator responses in the elderly.


2021 ◽  
Vol 35 (S1) ◽  
Author(s):  
Angelica Del Vecchio ◽  
Andrew Kuczmarski ◽  
Shane McGinty ◽  
Laura Welti ◽  
Joshua Hobson ◽  
...  

Author(s):  
Aelita Plinta ◽  
Pēteris Tretjakovs ◽  
Ināra Logina ◽  
Indra Miķelsone ◽  
Leons Blumfelds ◽  
...  

Abstract The aim of the study was to evaluate the changes in skin blood flow as a result of local heating tests in migraine patients during the interictal period, measured by laser Doppler perfusion imaging (LDI). The aim of the study was also to estimate the correlations between the results of these tests and interleukin (IL)-8 levels. Twelve migraine patients during their interictal period were compared with twelve healthy control subjects. Only women were included in the study. Both groups were matched with regard of their age, body mass index and blood pressure. For the purpose of measuring cutaneous microvascular blood flow, heating (+44 °C) of the dorsal side of the palm as a response to the local LDI was used. IL-8 was measured in serum by ELISA method. The findings suggested that migraine patients have a cutaneous vasomotor dysfunction during the interictal period. The results showed a significant decrease in the initial peak of vasodilation and the second peak of vasodilation (plateau phase). Also there were significant changes observed in the length of the time interval required to reach the first and second vasodilation peak. It is known that migraine patients have a shorter time interval to reach the first perfusion peak (axonal reflex-mediated) and longer time interval to reach the second peak (endothelium-dependent). The results confirmed the correlation between proinflammatory chemokine IL-8 levels, and the time interval till the second peak of blood flow in all study subjects.


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