Browsing by Author "Crandall, Craig G."

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    Combined Facial Heating and Inhalation of Hot Air Do Not Alter Thermoeffector Responses in Humans
    Wingo, Jonathan E.; Low, David A.; Keller, David M.; Kimura, Kenichi; Crandall, Craig G.; University of Alabama Tuscaloosa
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    Effect of elevated local temperature on cutaneous vasoconstrictor responsiveness in humans
    (American Physiological Society, 2009-02-01) Wingo, Jonathan E.; Low, David A.; Keller, David M.; Brothers, R. Matthew; Shibasaki, Manabu; Crandall, Craig G.; University of Texas System; University of Texas Southwestern Medical Center Dallas; Nara Womens University; University of Alabama Tuscaloosa
    Wingo JE, Low DA, Keller DM, Brothers RM, Shibasaki M, Crandall CG. Effect of elevated local temperature on cutaneous vasoconstrictor responsiveness in humans. J Appl Physiol 106: 571-575, 2009. First published December 4, 2008; doi: 10.1152/japplphysiol.91249.2008.-Cutaneous vascular conductance (CVC) increases in response to local skin heating. Although attenuation of vasoconstrictor responsiveness due to local heating has been demonstrated, the mechanism(s) responsible for this attenuation remains unclear. Nitric oxide has been shown to at least partially contribute to this response, but other mechanisms also may be involved. The purpose of this study was to test the hypothesis that local heating diminishes cutaneous vasoconstrictor responsiveness through a nitric oxide-independent mechanism by altering postsynaptic reactivity to norepinephrine. A follow-up protocol tested the hypothesis that local heating attenuates the presynaptic release of neurotransmitters that cause vasoconstriction, also via non-nitric oxide mechanisms. In protocol I, CVC was assessed in eight subjects during administration of increasing doses of norepinephrine (via intradermal microdialysis) at adjacent sites separately heated to 34 degrees C and 40 degrees C. In protocol II, which was identical to, but separate from, protocol I, CVC was assessed in seven subjects during administration of increasing doses of tyramine, which causes release of neurotransmitters from adrenergic nerves. At each site for both protocols, nitric oxide synthesis was inhibited (via microdialysis administration of N-G-nitro-L-arginine methyl ester) and flow was matched (via microdialysis administration of adenosine); therefore, temperature was the only variable that differed between the sites. For both protocols, nonlinear regression analysis revealed no difference (P > 0.05) in the effective drug concentration causing 50% of the vasoconstrictor response. Minimum CVC [6.3 +/- 2.0 and 9.0 +/- 4.0% of peak CVC (mean +/- SD) for protocol 1 and 19.3 +/- 9.3 and 20.5 +/- 11.9% of peak CVC for protocol II at 34 degrees C and 40 degrees C sites, respectively] was not different between sites. Independent of nitric oxide, local skin heating to 40 degrees C does not attenuate adrenergically mediated cutaneous vasoconstriction through pre- or postsynaptic mechanisms.
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    Heat acclimation of an adult female with a large surface area of grafted skin
    (Lippincott Williams & Wilkins, 2008-09-01) Wingo, Jonathan E.; Low, David A.; Keller, David M.; Davis, Scott L.; Kowalske, Karen J.; Purdue, Gary F.; Hunt, John L.; Crandall, Craig G.; University of Texas System; University of Texas Southwestern Medical Center Dallas; University of Alabama Tuscaloosa
    Grafted skin has impaired blood flow and sweating responses necessary for heat dissipation. Heat acclimation improves temperature regulation in healthy individuals, but it is unknown whether heat acclimation improves temperature regulation of individuals with large areas of grafted skin. A 33-year-old woman with 75% total body surface area grafted skin 14 years postinjury performed upright cycling exercise at 45% peak oxygen uptake (50 W) for seven consecutive days in a climatic chamber set to 40 degrees C and 30% relative humidity. The daily goal was for this patient to exercise 90 minutes (with a 5-minute break at minute 45); however, exercise was stopped when an internal temperature (T.) limit of 39.5 degrees C was reached. The T-c limit was reached during minute 46 of exercise on day 1 of acclimation, but not until minute 65 of exercise oil day 7 of acclimation. The increases in T-c and heart rate during the first 45 minutes of exercise (the minimum duration completed for all acclimation bouts) were progressively mitigated with successive days of heat acclimation. Sweat sensitivity (the increase in sweat rate per 1 degrees C increase in T-c) in an area of uninjured skin increased by similar to 30% oil acclimation clay 7 relative to day 1. Heat acclimation improved thermal tolerance of this patient with a large area of grafted skin, which could increase safety and comfort during thermal stress and/or exercise.
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    Intradermal Administration of ATP Does Not Mitigate Tyramine-Stimulated Vasoconstriction in Human Skin
    Wingo, Jonathan E.; Brothers, R. Matthew; Coso, Juan Del; Crandall, Craig G.; University of Alabama Tuscaloosa
    Cutaneous vasodilation associated with whole-body heat stress occurs via withdrawal of adrenergic vasoconstriction and engagement of cholinergic 'active' vasodilation, the latter of which attenuates cutaneous vasoconstrictor responsiveness. However, the precise neurotransmitter(s) responsible for this sympatholytic-like effect remain unknown. In skeletal muscle, ATP inhibits adrenergically mediated vasoconstriction. ATP also may be responsible for attenuating cutaneous vasoconstriction since it is coreleased from cholinergic neurons. The effect of ATP on cutaneous vasoconstrictor responsiveness, however, has not been investigated. Accordingly, this study tested the hypothesis that ATP inhibits adrenergically mediated cutaneous vasoconstriction. To accomplish this objective, four microdialysis probes were inserted in dorsal forearm skin of 11 healthy individuals (mean [+ or -] SD; 35 [+ or -] 11 years). Local temperature at each site was clamped at 34[degrees]C throughout the protocol. Skin blood flow was indexed by laser-Doppler flowmetry and was used to calculate cutaneous vascular conductance (CVC; laser-Doppler-derived flux/mean arterial pressure), which was normalized to peak CVC achieved with sodium nitroprusside infusion combined with local skin heating to ~42[degrees]C. Two membranes were perfused with 30 mM ATP, while the other two membranes were flow matched via administration of 2.8 mM adenosine to serve as control sites. After achieving stable baselines, 1 x [10.sup.-4] M tyramine was administered at all sites, while ATP and adenosine continued to be infused at their respective sites. ATP and adenosine infusion increased CVC from baseline by 35 [+ or -] 26% [CVC.sub.peak] units and by 36 [+ or -] 15% [CVC.sub.peak] units, respectively (P = 0.75). Tyramine decreased CVC similarly (by about one-third) at all sites (P < 0.001 for main effect and P = 0.32 for interaction). These findings indicate that unlike in skeletal muscle, ATP does not attenuate tyramine-stimulated vasoconstriction in human skin.
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    Skin Blood Flow and Local Temperature Independently Modify Sweat Rate During Passive Heat Stress in Humans
    Wingo, Jonathan E.; Low, David A.; Keller, David M.; Brothers, R. Matthew; Shibasaki, Manabu; Crandall, Craig G.; University of Alabama Tuscaloosa
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    Sympathetic nerve activity and whole body heat stress in humans
    (American Psyiological Society, 2011) Low, David A.; Keller, David M.; Wingo, Jonathan E.; Brothers, R. Matthew; Crandall, Craig G.; University of Texas Southwestern Medical Center Dallas; University of Texas Arlington; University of Alabama Tuscaloosa; University of Texas Austin
    Low DA, Keller DM, Wingo JE, Brothers RM, Crandall CG. Sympathetic nerve activity and whole body heat stress in humans. J Appl Physiol 111: 1329-1334, 2011. First published August 25, 2011; doi:10.1152/japplphysiol.00498.2011.-We and others have shown that moderate passive whole body heating (i.e., increased internal temperature similar to 0.7 degrees C) increases muscle (MSNA) and skin sympathetic nerve activity (SSNA). It is unknown, however, if MSNA and/or SSNA continue to increase with more severe passive whole body heating or whether these responses plateau following moderate heating. The aim of this investigation was to test the hypothesis that MSNA and SSNA continue to increase from a moderate to a more severe heat stress. Thirteen subjects, dressed in a water-perfused suit, underwent at least one passive heat stress that increased internal temperature similar to 1.3 degrees C, while either MSNA (n = 8) or SSNA (n = 8) was continuously recorded. Heat stress significantly increased mean skin temperature (Delta similar to 5 degrees C, P < 0.001), internal temperature (Delta similar to 1.3 degrees C, P < 0.001), mean body temperature (Delta similar to 2.0 C, P < 0.001), heart rate (Delta similar to 40 beats/min, P < 0.001), and cutaneous vascular conductance [Delta similar to 1.1 arbitrary units (AU)/mmHg, P < 0.001]. Mean arterial blood pressure was well maintained (P = 0.52). Relative to baseline, MSNA increased midway through heat stress (Delta core temperature 0.63 +/- 0.01 degrees C) when expressed as burst frequency (26 +/- 14 to 45 +/- 16 bursts/min, P = 0.001), burst incidence (39 +/- 13 to 48 +/- 14 bursts/100 cardiac cyles, P = 0.03), or total activity (317 +/- 170 to 489 +/- 150 units/min, P = 0.02) and continued to increase until the end of heat stress (burst frequency: 61 +/- 15 bursts/min, P = 0.01; burst incidence: 56 +/- 11 bursts/100 cardiac cyles, P = 0.04; total activity: 648 +/- 158 units/min, P = 0.01) relative to the mid-heating stage. Similarly, SSNA (total activity) increased midway through the heat stress (normothermia; 1,486 +/- 472 to mid heat stress 6,467 +/- 5,256 units/min, P = 0.03) and continued to increase until the end of heat stress (11,217 +/- 6,684 units/min, P = 0.002 vs. mid-heat stress). These results indicate that both MSNA and SSNA continue to increase as internal temperature is elevated above previously reported values.