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neurogenic inflammation/albumina
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Pagina 1 a partire dal 48 risultati
The use of radiolabelled human serum albumin and SPECT/MRI co-registration to study inflammation in the cavernous sinus of cluster headache patients.
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A sterile inflammation in the cavernous sinus was hypothesized to underlie cluster headache (CH). Neurogenic inflammation is accompanied by the extravasation of plasma proteins in the surrounding tissue. We tested the hypothesis of an inflammatory process in the cavernous sinus in CH patients using
Dose-dependent effects of capsaicin nasal challenge: in vivo evidence of human airway neurogenic inflammation.
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BACKGROUND
Nerve involvement has been implicated in the pathophysiology of chronic respiratory inflammatory diseases. Peptidergic nerve stimulation has been shown to induce leukocyte activation and plasma extravasation in the airways of various animal species. The occurrence of this phenomenon of
Replication-deficient adenoviral vector for gene transfer potentiates airway neurogenic inflammation.
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Human trials for the treatment of cystic fibrosis lung disease with adenoviral vectors have been complicated by acute inflammatory reactions of unknown etiology. Because replicating respiratory viruses can potentiate tachykinin-mediated neurogenic inflammatory responses in airways, we studied
Leukotrienes mediate neurogenic inflammation in lungs of young rats infected with respiratory syncytial virus.
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Respiratory syncytial virus (RSV) infection potentiates neurogenic inflammation in rat airways. Because some vascular effects of sensory nerves are mediated by cysteinyl leukotrienes (cysLTs), we studied whether the receptor antagonist montelukast inhibits neurogenic plasma extravasation in
Neurogenic inflammation, vascular permeability, and mast cells.
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Electrical stimulation (ES) of sensory nerves causes increased vascular permeability and vasodilatation, a process known as neurogenic inflammation. The purpose of this study was to assess the role of mast cells in neurogenic inflammation induced by ES of sensory nerves. ES of the rat saphenous
Targeting classical but not neurogenic inflammation reduces peritumoral oedema in secondary brain tumours.
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Dexamethasone, the standard treatment for peritumoral brain oedema, inhibits classical inflammation. Neurogenic inflammation, which acts via substance P (SP), has been implicated in vasogenic oedema in animal models of CNS injury. SP is elevated within and outside CNS tumours. This study
[Neurogenic inflammation and area of involvement of the facial nerve of the rat].
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Antidromic electrical stimulation of sensory nerves produces vascular hyperpermeability, plasma protein extravasation and oedema. The initial phase of this inflammatory reaction is induced by the release of the neuropeptides CGRP, SP and NKA; the later phase is induced by mast cells. In previous
Neurogenic inflammation and lowering of interstitial fluid pressure in rat trachea is inhibited by alpha-trinositol.
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The effect of alpha-trinositol (D-myoinositol-1,2,6-triphosphate) on edema formation and capillary permeability in neurogenically induced inflammatory edema was investigated in rat trachea. Interstitial fluid pressure (Pif) was studied, since increased negativity of Pif contributes to edema
Is there a correlation between spreading depression, neurogenic inflammation, and nociception that might cause migraine headache?
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The time course of propagation of scotoma and blood flow changes during migraine aura parallels the phenomenon of cortical spreading depression (CSD). It was proposed that CSD generates a sterile neurogenic inflammation in the meninges, which may then lead to the activation or sensitization of
Neuropeptide release augments serum albumin loss and reduces ultrafiltration in peritoneal dialysis.
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BACKGROUND
The triggers of the acute local inflammatory response to peritoneal dialysis (PD) fluid exposure remain unknown. In the present study, we investigated the effects of neurogenic inflammation and mast cell degranulation on water and solute transport in experimental PD.
METHODS
Single 2-hour
Neurogenic inflammation after traumatic brain injury and its potentiation of classical inflammation.
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The neuroinflammatory response following traumatic brain injury (TBI) is known to be a key secondary injury factor that can drive ongoing neuronal injury. Despite this, treatments that have targeted aspects of the inflammatory pathway have not shown significant efficacy in clinical trials.
We
Exaggerated neurogenic inflammation and substance P receptor upregulation in RSV-infected weanling rats.
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Respiratory syncytial virus (RSV) infection in adult rats causes exaggerated inflammation after sensory nerve stimulation in the extrapulmonary, but not in the intrapulmonary airways. The goal of this study was to analyze neurogenic inflammation in weanling F-344 rats infected with RSV 18 +/- 2 d
Neurogenic inflammation in the airways. I. Neurogenic stimulation induces plasma protein extravasation into the rat airway lumen.
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Activation of sensory nerves in rodent airways results in microvascular permeability and edema formation, presumably due to release of vasoactive neuropeptides from the nerve endings. We examined the possibility that neurogenic stimulation may also induce movement of plasma proteins into the airway
Essential role for nitric oxide in neurogenic inflammation in rat cutaneous microcirculation. Evidence for an endothelium-independent mechanism.
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The possible modulatory role of nitric oxide (NO) in neurogenic edema formation in rat paw skin, induced by electrical stimulation of the saphenous nerve, was investigated by using two NO synthase inhibitors, NG-nitro-L-arginine methyl ester (L-NAME) and 7-nitroindazole (7-NI). Both L-NAME (100
Neurogenic inflammation, vascular permeability, and mast cells. Capsaicin desensitization fails to influence IgE-anti-DNP induced vascular permeability in rat airways.
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Mast cells and neuropeptide-containing nerves occur in close proximity throughout the mucosa. The vasodilation that characteristically occurs after mast cell mediator release in skin is dependent upon sensory nerve activation with neuropeptide release. It was therefore of interest to examine the
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