ライフサイエンスコーパス: axon reflex

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1 h acute CRPS I is most likely mediated by an axon reflex and that alpha-adrenoreceptor supersensitivi

2 sitizing the sensory nerves that mediate the axon reflex associated with rapid vasodilatation.

3 enaline on the temperature threshold for the axon reflex during gradual local heating.

4 units and will make the main contribution to axon reflex flare and other neurogenic inflammatory resp

5 on of thermal thresholds and reduced sensory axon-reflex flare responses in affected skin correlated

6 eased nerve fibres in the subepidermis, e.g. axon-reflex flux units (means+/-SEM) for no detectable i

7 suggesting that the effects were not merely axon reflexes generated by stimulation of corticospinal

8 whole-body heat stress and during peripheral axon reflex-mediated, local responses to skin warming in

9 SP is the primary mediator of an axon reflex mediating neurogenic inflammation in the int

10 In agreement with the axon reflex model, spread of flare was restricted to the

11 us, suggesting that they may form part of an axon reflex or similar mechanism.

12 ntribute to the temperature threshold of the axon reflex response during gradual local heating of the

13 e noradrenaline infusion, also abolished the axon reflex response in all subjects.

14 Compared to control skin sites, the axon reflex response was shifted to a higher temperature

15 eat stress, but not during locally mediated, axon reflex responses to local skin warming.

16 Reduced nicotine-induced axon-reflex sweating was correlated with decreased inner

17 he methodology of the quantitative sudomotor axon reflex test (QSART).

18 on as measured by the Quantitative Sudomotor Axon Reflex Test, most significantly in the foot; the sc

19 ipants also completed quantitative sudomotor axon reflex testing, quantitative sensory testing, the n

20 ose noradrenaline infusion alone shifted the axon reflex to a significantly lower temperature thresho

21 d contributions of spinal reflexes or distal axon reflexes to the distribution of tension to multiple

22 As loss of nociception and axon-reflex vasodilation contribute to diabetic foot ulc

23 ion between NGF depletion and decreased skin axon-reflex vasodilation, mediated by small sensory fibe

24 evident as a reduced ability to propagate an axon-reflex vasodilator response when challenged with hi

25 tion of heat is thought to be mediated by an axon reflex, which is dependent on intact cutaneous sens

26 d flow response to rapid local heating is an axon reflex, which may be mediated by calcitonin gene-re

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