Articles: postganglionic-sympathetic-fibers.
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Chemically-induced quantitative sudomotor axon reflex test (QSART) and quantitative sensory testing (QST) are established clinical tools to assess thin fiber function in humans. We investigated stimulus-response functions to transcutaneous electrical stimuli of different current intensity (3.75 to 10mA) and pulse frequency (5 to 100Hz) comparing sweat output (ml/h/m(2)) and pain intensity (numeric rating scale [NRS], 0-10). Efferent sudomotor and afferent nociceptive responses were recorded after a 30s electrical stimulation period of distal (hand and foot) and proximal (forearm and thorax) body sites with 3 repetitive measures per body site. ⋯ Sudomotor activity, but not pain ratings, was significantly different between the body sites (p<0.05, ANOVA) with maximum sweat responses obtained at the ventral forearm. Varying response patterns for higher stimulation frequencies between sweating (peak maximum at 20Hz) and pain (maximum at 100Hz) might indicate differential axonal properties of sympathetic efferent and nociceptive afferent fibers. Electrically induced QSART could be a useful explorative and clinical method to indirectly study characteristics of frequency-dependent axonal excitability changes of sudomotor fibers.
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Iontophoresis of α(1)-adrenoceptor agonists in the human forearm evoke axon reflex vasodilatation, possibly due to an accumulation of inflammatory agents at the site of iontophoresis. To investigate this possibility, skin sites in the forearm of healthy participants were treated with an anti-inflammatory gel containing ibuprofen 5% before the iontophoresis of the α(1)-adrenoceptor agonist phenylephrine (350μA for 3min). Red cell flux was measured with laser Doppler flowmetry at the site of iontophoresis and 8mm away in the region of axon reflex vasodilatation. ⋯ Axon reflex vasodilatation to phenylephrine was unaffected by variations in blood flow at the site of phenylephrine iontophoresis, but was reduced by ibuprofen pretreatment and abolished by local anaesthetic pretreatment. These findings suggest that prostaglandin synthesis at the site of iontophoresis contributes to but does not account entirely for axon reflex vasodilatation to phenylephrine. Alpha-1 adrenoceptor mediation of axon reflexes could play a role in aberrant sensory-sympathetic coupling in neuro-inflammatory diseases.
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The aim of this study was to determine whether pre-treatment of human skin with the alpha(1)-adrenoceptor antagonist terazosin would block vasoconstrictor responses and axon-reflex vasodilatation to the alpha(1)-adrenoceptor agonist methoxamine. Drugs were administered by iontophoresis into the skin of the forearm of 15 healthy participants, and skin blood flow was monitored with a laser Doppler flow probe at the site of methoxamine iontophoresis (to monitor direct vasoconstrictor responses) or 5-10 mm from the site of methoxamine iontophoresis (to monitor axon-reflex vasodilatation). ⋯ Pre-treatment with terazosin blocked vasoconstrictor responses to increasing doses of methoxamine, and also blocked vasodilatation several mm from the site of terazosin and methoxamine administration. These findings support the view that alpha(1)-adrenoceptors play a role in generating axon-reflex vasodilatation, and thus might contribute to local vascular disturbances in acute and chronic inflammation.
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A 54-year-old woman who underwent chest tube placement after a lung biopsy was found on the first postoperative day to have ipsilateral ptosis and miosis, suggesting a Horner syndrome. A chest CT scan showed that the tip of the chest tube was apposed to the stellate ganglion. ⋯ We propose that the Horner syndrome arose as a result of pressure on the stellate ganglion, which interrupted neural conduction but did not sever the sympathetic pathway ("neurapraxia"). Whether prompt repositioning of the chest tube was critical in reversing the Horner syndrome is uncertain.
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Chronic pain that responds to antisympathetic treatments and alpha-adrenergic antagonists is clinically referred to as sympathetically maintained pain. Animal models of neuropathic pain have shown mixed results in terms of antinociceptive effectiveness of antisympathetic agents. The effectiveness of these agents have not been yet investigated in animal models of complex regional pain syndrome-type 1 (CRPS-I). In this study, we examined the effectiveness of antisympathetic agents and sympathetic vasoconstrictor antagonists, as well as agents that are vasodilators, in relieving mechanical allodynia in a recently developed animal model of CRPS-I (chronic postischemia pain or CPIP) produced by 3 hours of hind paw ischemia-reperfusion injury. Systemic guanethidine, phentolamine, clonidine, and prazosin are effective in reducing mechanical allodynia particularly at 2 days after reperfusion, and less so at 7 days after reperfusion. A nitric oxide donor vasodilator, SIN-1, also reduces mechanical allodynia more effectively at 2 days after reperfusion, but not at 7 days after reperfusion. These results suggest that the pain of CPIP, and possibly also CRPS-I, is relieved by reducing sympathetically mediated vasoconstriction, or enhancing vasodilatation. ⋯ The results of this study indicate that sympathetic block, or administration of alpha(1)-adrenergic antagonists, clonidine, or a nitric oxide donor, relieve allodynia in an animal model of CRPS-I. Thus, the pain of CRPS-I may depend on enhanced vasoconstrictor responsiveness, which may be relieved by blocking sympathetic efferent-dependent vasoconstriction, or by enhancing nitric oxide-dependent vasodilatation.