Whole-Body Heating Decreases Skin Vascular Response to Low Orthostatic Stress in the Lower Extremities

Yamazaki, Fumio; Nakayama, Yoshiro; Sone, Ryoko

doi:10.2170/physiolsci.rp000406

Cited by 13 publications

(16 citation statements)

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“…Unchanged skin sympathetic nerve activity in response to baroreceptor unloading has been observed in normothermic and heat-stressed humans (7, 39, 41). However, significant cutaneous vasoconstrictor responses in the forearm and palm at the heart level during orthostatic stress in these thermal conditions (6,34,45,47,48) suggest participation of sympathetic vasoconstrictor function in the responses without a detectable change in the neural signal. Unfortunately, it is unknown whether sympathetic adrenergic vasoconstrictor responsiveness in the skin shows a regional difference between the upper and lower limbs, since blood flow measured in the previous reports represents a composite of flow in both muscle and skin (15,22,38).…”

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confidence: 97%

“…IN HUMANS, peripheral vasoconstrictor responses to upright posture show heterogeneity between the upper and lower limbs (14,16,22,48). The findings from previous studies suggest that the leg vasculature is more responsive to orthostatic stimulation than the arm vasculature.…”

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confidence: 99%

“…These findings suggest that the cutaneous vasoconstrictor responsiveness to exogenous NE is greater in the legs than in the arms due to a higher ␣1-and ␣2-adrenoceptor reactivity, while the ␤-adrenoceptor function plays a minor role in regional differences in adrenergic vasoconstriction in normothermic humans. skin blood flow; exogenous norepinephrine; ␣-adrenergic receptor; ␤-adrenergic receptor; microdialysis IN HUMANS, peripheral vasoconstrictor responses to upright posture show heterogeneity between the upper and lower limbs (14,16,22,48). The findings from previous studies suggest that the leg vasculature is more responsive to orthostatic stimulation than the arm vasculature.…”

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confidence: 99%

“…With regard to adrenergic receptor responsiveness, Pawelczyk and Levine (29) reported a relatively greater vasoconstrictor response to ␣ 1 -adrenergic receptor stimulation in the calf compared with the forearm. In contrast, the vasodilator response to ␤-adrenergic receptor stimulation evaluated based on the percent change in maximal vascular conductance did not differ between the arm and leg (29), and the vasodilator response evaluated based on the percent change in baseline blood flow was smaller in the leg (15).Vasomotor control in the skin could be involved in the maintenance of arterial blood pressure during orthostatic stress, especially in hyperthermia given the large fraction of vascular conductance of the skin relative to the entire vasculature (5,9,18,47,48). Unchanged skin sympathetic nerve activity in response to baroreceptor unloading has been observed in normothermic and heat-stressed humans (7, 39, 41).…”

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confidence: 99%

“…Vasomotor control in the skin could be involved in the maintenance of arterial blood pressure during orthostatic stress, especially in hyperthermia given the large fraction of vascular conductance of the skin relative to the entire vasculature (5,9,18,47,48). Unchanged skin sympathetic nerve activity in response to baroreceptor unloading has been observed in normothermic and heat-stressed humans (7, 39, 41).…”

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Limb-specific differences in the skin vascular responsiveness to adrenergic agonists

Yamazaki

Yuge

2011

Journal of Applied Physiology

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Yamazaki F, Yuge N. Limb-specific differences in the skin vascular responsiveness to adrenergic agonists. J Appl Physiol 111: 170-176, 2011. First published April 28, 2011 doi:10.1152/japplphysiol.00068.2011In this study, to test the hypothesis that adrenergic vasoconstrictor responses of the legs are greater compared with the arms in human skin, cutaneous vascular conductance (CVC) in the forearm and calf were compared during the infusion of adrenergic agonists in healthy young volunteers. Under normothermic conditions, norepinephrine (NE, ␣-and ␤-agonist, 1 ϫ 10 Ϫ8 to 1 ϫ 10 Ϫ2 M), phenylephrine (PHE, ␣1-agonist, 1 ϫ 10 Ϫ8 to 1 ϫ 10 Ϫ2 M), dexmedetomidine (DEX, ␣2-agonist, 1 ϫ 10 Ϫ9 to 1 ϫ 10 Ϫ4 M), and isoproterenol (ISO, ␤-agonist, 1 ϫ 10 Ϫ8 to 1 ϫ 10 Ϫ3 M) were administered by intradermal microdialysis. Skin blood flow (SkBF) was measured by laserDoppler flowmetry, and the local temperature at SkBF-measuring sites was maintained at 34°C throughout the experiments. CVC was calculated as the ratio of SkBF to blood pressure and expressed relative to the baseline value before drug infusion. The dose of NE at the onset of vasoconstriction and the effective dose (ED50) resulting in 50% of the maximal vasoconstrictor response for NE were lower (P Ͻ 0.001) in the calf than forearm. The ED50 for PHE and DEX was also lower (P Ͻ 0.05) in the calf than forearm. Increases in CVC in response to ISO were potentially smaller in the calf, but the statistical differences in the responses were dependent on the expressions of CVC. These findings suggest that the cutaneous vasoconstrictor responsiveness to exogenous NE is greater in the legs than in the arms due to a higher ␣1-and ␣2-adrenoceptor reactivity, while the ␤-adrenoceptor function plays a minor role in regional differences in adrenergic vasoconstriction in normothermic humans. skin blood flow; exogenous norepinephrine; ␣-adrenergic receptor; ␤-adrenergic receptor; microdialysis IN HUMANS, peripheral vasoconstrictor responses to upright posture show heterogeneity between the upper and lower limbs (14,16,22,48). The findings from previous studies suggest that the leg vasculature is more responsive to orthostatic stimulation than the arm vasculature. The augmented vasoconstrictor response observed in the human lower-leg vasculature is influenced by sympathetic and local mechanisms (14,22,24,38) and could play an important regulatory role by limiting the degree to which blood accumulates in the legs during orthostatic stress (29,30).The vasoconstrictor response to the upright posture is via reflex and nonreflex (e.g., venoarteriolar response) mechanisms. The reflex vasoconstriction is influenced by centrally driven activity in sympathetic vasoconstrictor nerves and postjunctional adrenergic receptor responsiveness. With regard to the central sympathetic outflow, similar increases in muscle sympathetic nerve activity have been shown in the arm and leg during orthostatic stress (14, 31). In addition, similar increases in regional norepinephrine (NE) spillover have been re...

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Limb-specific differences in the skin vascular responsiveness to adrenergic agonists

Yamazaki

Yuge

2011

Journal of Applied Physiology

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Cerebral Vascular Control and Metabolism in Heat Stress

Bain

Nybo

Ainslie

2015

Comprehensive Physiology

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This review provides an in-depth update on the impact of heat stress on cerebrovascular functioning. The regulation of cerebral temperature, blood flow, and metabolism are discussed. We further provide an overview of vascular permeability, the neurocognitive changes, and the key clinical implications and pathologies known to confound cerebral functioning during hyperthermia. A reduction in cerebral blood flow (CBF), derived primarily from a respiratory-induced alkalosis, underscores the cerebrovascular changes to hyperthermia. Arterial pressures may also become compromised because of reduced peripheral resistance secondary to skin vasodilatation. Therefore, when hyperthermia is combined with conditions that increase cardiovascular strain, for example, orthostasis or dehydration, the inability to preserve cerebral perfusion pressure further reduces CBF. A reduced cerebral perfusion pressure is in turn the primary mechanism for impaired tolerance to orthostatic challenges. Any reduction in CBF attenuates the brain's convective heat loss, while the hyperthermic-induced increase in metabolic rate increases the cerebral heat gain. This paradoxical uncoupling of CBF to metabolism increases brain temperature, and potentiates a condition whereby cerebral oxygenation may be compromised. With levels of experimentally viable passive hyperthermia (up to 39.5-40.0 °C core temperature), the associated reduction in CBF (∼ 30%) and increase in cerebral metabolic demand (∼ 10%) is likely compensated by increases in cerebral oxygen extraction. However, severe increases in whole-body and brain temperature may increase blood-brain barrier permeability, potentially leading to cerebral vasogenic edema. The cerebrovascular challenges associated with hyperthermia are of paramount importance for populations with compromised thermoregulatory control--for example, spinal cord injury, elderly, and those with preexisting cardiovascular diseases.

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Thermal sensation during mild hyperthermia is modulated by acute postural change in humans

et al. 2016

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Thermal sensation represents the primary stimulus for behavioral and autonomic thermoregulation. We assessed whether the sensation of skin and core temperatures for the driving force of behavioral thermoregulation was modified by postural change from the supine (Sup) to sitting (Sit) during mild hyperthermia. Seventeen healthy young men underwent measurements of noticeable increase and decrease (±0.1 °C/s) of skin temperature (thresholds of warm and cold sensation on the skin, 6.25 cm of area) at the forearm and chest and of the whole-body warm sensation in the Sup and Sit during normothermia (NT; esophageal temperature (T), ∼36.6 °C) and mild hyperthermia (HT; T, ∼37.2 °C; lower legs immersion in 42 °C of water). The threshold for cold sensation on the skin at chest was lower during HT than NT in the Sit (P < 0.05) but not in Sup, and at the forearm was lower during HT than NT in the Sup and further in Sit (both, P < 0.05), with interactive effects of temperature (NT vs. HT) × posture (Sup vs. Sit) (chest, P = 0.08; forearm, P < 0.05). The threshold for warm sensation on the skin at both sites remained unchanged with changes in body posture or temperature. The whole-body warm sensation was higher during HT than NT in both postures and higher in the Sit than Sup during both NT and HT (all, P < 0.05). Thus, thermal sensation during mild hyperthermia is modulated by postural change from supine to sitting to sense lesser cold on the skin and more whole-body warmth.

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Whole-Body Heating Decreases Skin Vascular Response to Low Orthostatic Stress in the Lower Extremities

Cited by 13 publications

References 35 publications

Limb-specific differences in the skin vascular responsiveness to adrenergic agonists

Limb-specific differences in the skin vascular responsiveness to adrenergic agonists

Cerebral Vascular Control and Metabolism in Heat Stress

Thermal sensation during mild hyperthermia is modulated by acute postural change in humans

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