Characterization of ruthenium red as an inhibitor of neurogenic inflammation in the rat trachea

James J. Brokaw, Gary White

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

1. 1. We investigated the ability of ruthenium red, an inorganic dye with capsaicin antagonist properties, to inhibit capsaicin-induced plasma extravasation in the rat trachea. 2. 2. The amount of plasma extravasation produced by intravenous capsaicin was reduced dose-dependently by i.v. ruthenium red. Complete inhibition was achieved with a dose of 5 μmol/kg. 3. 3. The inhibitory effect of ruthenium red persisted for at least 16 hr after its administration, but was not present 24 hr later. 4. 4. Ruthenium red did not reduce the amount of plasma extravasation produced by electrical stimulation of the vagus nerve, nor the amount produced by intravenous substance P or platelet-activating factor. 5. 5. Prior exposure to a high dose of capsaicin reduced the amount of plasma extravasation produced by a second capsaicin exposure 48 hr later. However, giving ruthenium red 30 min before the initial capsaicin exposure largely prevented this loss of sensory nerve function. 6. 6. We conclude that systemic administration of ruthenium red produces long-lasting, selective, and reversible inhibition of capsaicin-induced plasma extravasation in the rat trachea. Moreover, ruthenium red attenuates the long-term, desensitizing effect of capsaicin on sensory nerves.

Original languageEnglish
Pages (from-to)327-331
Number of pages5
JournalGeneral Pharmacology
Volume26
Issue number2
DOIs
StatePublished - 1995

Fingerprint

Neurogenic Inflammation
Ruthenium Red
Capsaicin
Trachea
Aptitude
Vagus Nerve
Platelet Activating Factor
Substance P
Electric Stimulation
Coloring Agents

Keywords

  • airways
  • capsaicin
  • Ruthenium red
  • vascular permeability

ASJC Scopus subject areas

  • Pharmacology

Cite this

Characterization of ruthenium red as an inhibitor of neurogenic inflammation in the rat trachea. / Brokaw, James J.; White, Gary.

In: General Pharmacology, Vol. 26, No. 2, 1995, p. 327-331.

Research output: Contribution to journalArticle

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