1957
Physiologic Studies in Atopic Dermatitis (Disseminated Neurodermatitis)
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1958
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Cited by 15 publications
(8 citation statements)
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Abstract
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“…Parallel action potentials spread antidromically via axon collaterals leading to stimulation of nerve fibers with concomitant release of neuropeptides such as substance P or calcitonin gene related peptide. The flare reaction is visible on the skin surface and can be evaluated as the efferent part of the axon reflex (36–39).…”
Section: Discussion
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confidence: 99%
Abstract
Smart CitationsHow this paper cites the one you are viewing
“…Parallel action potentials spread antidromically via axon collaterals leading to stimulation of nerve fibers with concomitant release of neuropeptides such as substance P or calcitonin gene related peptide. The flare reaction is visible on the skin surface and can be evaluated as the efferent part of the axon reflex (36–39).…”
Section: Discussion
mentioning
confidence: 99%
Abstract
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“…Reactions to several pharmacological agents have also been demonstrated in atopic dermatitis sufferers. Lobitz and Campbell (1953) found that intradermal injection with acetylcholine or methacholine produced a paradoxical white blanched area inside the flare in atopic dermatitis skin, instead of the usual reddening. This reaction has been referred to as delayed blanch.…”
Section: Pharmacological Abnormalities
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confidence: 95%
“…The first component, an erythematous line develops in 3 to 15 seconds along the line of stroking, and is due to dilatation of the precapillary sphincter by the action of vasodilator substances such as histamine and polypeptides (Whitlock, 1976). The "flare" response develops a few seconds after the red line and is due to the dilatation of the arterioles in an axon-reflex (Lobitz & Campbell, 1953). The third component is the "weal" response which develops one to three minutes after the red line, which it replaces.…”
Section: Physiological and Pharmacological Abnormalities
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confidence: 99%
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“…SAXL Die E ntstehung der Hautm anifestation der atopischen Derm atitis ist Gegenstand einer Reihe von Arbeitshypothesen. Es ist wahr scheinlich, daß die Morphe des endogenen Ekzems der Neurodermitis durch einen Mechanismus verm ittelt wird, in dem einerseits vaskuläre Erscheinungen [1], wie verspätetes Auslösen des Auslöschphänomens (Delayed-blanch-Phänomen) nach Acetylcholin [2,3,4], atypische Reaktion nach Nikotinsäureestern [5,6,7,8,9], andererseits Abwei chungen in der Schweißabsonderung der ekkrinen Schweißdrüsen (Hypohidrosc, Bradyhidrose) [10] und Veränderungen im Verhor nungsprozeß und in der Talgbildung (Symptom der trockenen H aut, der Kerose, Xerose, dry skin) [11,12,13] eine Rolle spielen. Es ist bisher fraglich, ob die ursprüngliche Ursache der Neurodermitis Reaginbindung in der H aut [14,15,16] und durch immunologische Reaktion hervorgerufenes Jucken [17,18] oder eine durch Schweiß retention verursachte Mikroinjektion von Antigenen in die Epidermis ist [19].…”
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