No effect of systemic isocapnic hypoxia on α-adrenergic vasoconstrictor responsiveness in human skin

Simmons, Grant H.; Fieger, Sarah M.; Wong, Brett J.; Halliwill, John R.

doi:10.1111/j.1748-1716.2010.02193.x

Cited by 9 publications

(15 citation statements)

References 32 publications

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“…Conversely, an increase in vascular responsiveness to sympathetic cotransmitters could be stimulated by local hypoxia. Unfortunately, the present data cannot conclusively distinguish between these potential mechanisms, and previous tests of cutaneous postjunctional vasoconstrictor responsiveness during hypoxia do not shed light on the function of non-noradrenergic vasoconstrictor mechanisms (Simmons et al 2011). Nevertheless, we believe that a central effect of hypoxia on nonnoradrenergic cutaneous vasoconstriction is the more likely explanation for two reasons.…”

Section: Cold-induced Vasoconstriction: Mechanisms Of the Hypoxic Effectcontrasting

confidence: 78%

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Cutaneous vascular and core temperature responses to sustained cold exposure in hypoxia

Simmons

Barrett-O’Keefe

Halliwill

2011

Experimental Physiology

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We tested the effect of hypoxia on cutaneous vascular regulation and defense of core temperature during cold exposure. Twelve subjects had two microdialysis fibres placed in the ventral forearm and were immersed to the sternum in a bathtub on parallel study days (normoxia and poikilocapnic hypoxia with an arterial O 2 saturation of 80%). One fibre served as the control (1 mm propranolol) and the other received 5 mm yohimbine (plus 1 mm propranolol) to block adrenergic receptors. Skin blood flow was assessed at each site (laser Doppler flowmetry), divided by mean arterial pressure to calculate cutaneous vascular conductance (CVC), and scaled to baseline. Cold exposure was first induced by a progressive reduction in water temperature from 36 to 23• C over 30 min to assess cutaneous vascular regulation, then by clamping the water temperature at 10• C for 45 min to test defense of core temperature. During normoxia, cold stress reduced CVC in control (−44 ± 4%) and yohimbine sites (−13 ± 7%; both P < 0.05 versus precooling). Hypoxia caused vasodilatation prior to cooling but resulted in greater reductions in CVC in control (−67 ± 7%) and yohimbine sites (−35 ± 11%) during cooling (both P < 0.05 versus precooling; both P < 0.05 versus normoxia). Core cooling rate during the second phase of cold exposure was unaffected by hypoxia (−1.81 ± 0.23• C h −1 in normoxia versus −1.97 ± 0.33• C h −1 in hypoxia; P > 0.05). We conclude that hypoxia increases cutaneous (non-noradrenergic) vasoconstriction during prolonged cold exposure, while core cooling rate is not consistently affected.

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Section: Cold-induced Vasoconstriction: Mechanisms Of the Hypoxic Effectcontrasting

confidence: 78%

“…The time course of drug delivery in this protocol was based on previous studies (Stephens et al 2004;Thompson & Kenney, 2004). We and others have shown that local blockade of the adrenergic system does not affect baseline skin blood flow in a thermoneutral environment (Stephens et al 2004;Simmons et al 2011).…”

Section: Methodsmentioning

confidence: 99%

Cutaneous vascular and core temperature responses to sustained cold exposure in hypoxia

Simmons

Barrett-O’Keefe

Halliwill

2011

Experimental Physiology

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“…Using similar methodology to the present study, a contributory role for NPY in the reflex cutaneous VC response was discovered by Stephens et al (2004), who demonstrated that intradermal microdialysis of a NPY Y 1 antagonist, BIBP-3226, attenuated the reflex VC to whole-body cooling. However, in other studies using the same antagonist during cooling (Thompson, 2005;Greaney et al 2015a) or hypoxia (Simmons et al 2011), there was no observed effect on the cutaneous VC response. However, in other studies using the same antagonist during cooling (Thompson, 2005;Greaney et al 2015a) or hypoxia (Simmons et al 2011), there was no observed effect on the cutaneous VC response.…”

Section: J a Lang And Othersmentioning

confidence: 74%

Evidence for a functional vasoconstrictor role for ATP in the human cutaneous microvasculature

Lang

Krajek

Smaller

2017

Experimental Physiology

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What is the central question of this study? In young adults, about half of the cold-related reduction in skin blood flow during cold exposure is mediated by noradrenaline, while the remainder is attributable to other substances co-released with noradrenaline that have yet to be identified. What is the main finding and its importance? Purinergic receptor blockade blunted the vasoconstriction response to whole-body cooling and to intradermal administration of tyramine. These results indicate that ATP is necessary to vasoconstrict blood vessels in the skin adequately and prevent heat loss in a cold environment. Noradrenaline is responsible for eliciting ∼60% of the reflex cutaneous vasoconstriction (VC) response in young adults, while the remainder is attributable to one or more unidentified co-released sympathetic adrenergic neurotransmitter(s). Inconsistent evidence has placed neuropeptide Y in this role; however, other putative cotransmitters have yet to be tested. We hypothesize that ATP contributes to the reflex cutaneous VC response. Two protocols were conducted in young adults (n = 10); both involved the placement of three microdialysis probes in forearm skin and whole-body cooling (skin temperature = 30.5°C). In protocol 1, the following solutions were infused: (i) lactated Ringer solution (control); (ii) 10 mm l-NAME; and (iii) purinergic receptor blockade with 1 mm suramin plus l-NAME. In protocol 2, the following solutions were infused: (i) lactated Ringer solution; (ii) suramin plus l-NAME; and (iii) suramin plus l-NAME plus adrenoreceptor blockade with 5 mm yohimbine plus 1 mm propranolol. Laser Doppler flux (LDF) was measured over each microdialysis site, and cutaneous vascular conductance (CVC) was calculated (CVC = LDF/MAP) and expressed as percentage changes from baseline (%ΔCVC ). l-NAME was used to block the vasodilatory influence of ATP and unmask the P X-mediated VC response to exogenous ATP infusion (-21 ± 6%ΔCVC ). During cooling, the VC response (control, -39 ± 8%ΔCVC ) was attenuated at the suramin site (-21 ± 4%ΔCVC ) and further blunted with combined adrenoreceptor blockade (-9 ± 3%ΔCVC ; P < 0.05). Compared with the control site (-22 ± 5%ΔCVC ), suramin inhibited pharmacologically induced VC to tyramine (-12 ± 6%ΔCVC ; P < 0.05), which displaces adrenergic neurotransmitters from axon terminals. These data indicate that ATP contributes to the cutaneous VC response in humans.

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“…With acute cold exposure in a laboratory setting, Simmons et al. [70–72] studied the effect of hypoxia on cutaneous vascular conductance during cold exposure. Data from these three studies are mixed, suggesting both increased and decreased cutaneous vasoconstriction in the forearm.…”

Section: Longitudinal Field Studiesmentioning

confidence: 99%

“…Based on field acclimation studies, one intriguing possibility is that hypoxic exposure itself, irrespective of cold exposure, potentiates CIVD response and local thermal response to cold. With acute cold exposure in a laboratory setting, Simmons et al [70][71][72] studied the effect of hypoxia on cutaneous vascular conductance during cold exposure. Data from these three studies are mixed, suggesting both increased and decreased cutaneous vasoconstriction in the forearm.…”

Section: Longitudinal Field Studiesmentioning

confidence: 99%

Dynamic Adaptation of the Peripheral Circulation to Cold Exposure

Cheung

Daanen

2011

Microcirculation

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Humans residing or working in cold environments exhibit a stronger cold-induced vasodilation (CIVD) reaction in the peripheral microvasculature than those living in warm regions of the world, leading to a general assumption that thermal responses to local cold exposure can be systematically improved by natural acclimatization or specific acclimation. However, it remains unclear whether this improved tolerance is actually due to systematic acclimatization, or alternately due to the genetic predisposition or self-selection for such occupations. Longitudinal studies of repeated extremity exposure to cold demonstrate only ambiguous adaptive responses. In field studies, general cold acclimation may lead to increased sympathetic activity that results in reduced finger blood flow. Laboratory studies offer more control over confounding parameters, but in most studies, no consistent changes in peripheral blood flow occur even after repeated exposure for several weeks. Most studies are performed on a limited amount of subjects only, and the variability of the CIVD response demands more subjects to obtain significant results. This review systematically surveys the trainability of CIVD, concluding that repeated local cold exposure does not alter circulatory dynamics in the peripheries, and that humans remain at risk of cold injuries even after extended stays in cold environments.

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No effect of systemic isocapnic hypoxia on α-adrenergic vasoconstrictor responsiveness in human skin

Abstract: We conclude that post-junctional α-adrenergic vasoconstrictor responsiveness is not affected by hypoxia in non-acral skin.

Cited by 9 publications

References 32 publications

Cutaneous vascular and core temperature responses to sustained cold exposure in hypoxia

Cutaneous vascular and core temperature responses to sustained cold exposure in hypoxia

Evidence for a functional vasoconstrictor role for ATP in the human cutaneous microvasculature

Dynamic Adaptation of the Peripheral Circulation to Cold Exposure

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