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C. Beauregard, D. Stephens, M. A. McLaughlin, D. A. Gamache, J. M. Yanni; Investigation of the Role of H2 Receptors in Histamine-Induced Conjunctival Hyperemia and Vascular Permeability. Invest. Ophthalmol. Vis. Sci. 2007;48(13):2304.
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The roles of the H1 and H2 histamine receptors in the conjunctiva has been controversial. It has been reported that conjunctival histamine-induced vascular permeability is mediated solely by H1, with no H2 involvement. However, combined use of H1 and H2 antagonists was shown to inhibit ocular redness (hyperemia) in response to topical histamine challenge, while either antagonist alone was ineffective. The current study investigates the independent roles of H1 and H2 receptors in conjunctival hyperemia and vascular permeability in histamine-challenged guinea pig models using receptor subtype-specific pharmacological agents.
To measure histamine-induced conjunctival vascular permeability male Hartley outbred guinea pigs were challenged with a subconjunctival injection of histamine one hour following intravenous injection of 1 ml Evans blue dye (1 mg/ml). Thirty minutes after histamine challenge, conjunctival vascular permeability was assessed ex vivo by measuring the area and color intensity stained with Evans blue dye. Test drugs were administered topically at various times prior to histamine challenge. To measure hyperemia, guinea pigs were topically challenged with histamine and scored for redness for up to 4 hrs post-challenge by a masked observer. Incidence of redness was determined in relation to pre-dosing baseline for each animal. Statistical differences between groups were determined using Dunnett's t-test or Χ2 test appropriate.
The H2-specific antagonists, ranitidine and famotidine, had no significant inhibitory effect on histamine-induced conjunctival vascular permeability with a 30 min pre-treatment interval, while the H1-specific antagonist, emedastine, significantly inhibited vascular permeability under the same conditions. Emedastine also significantly inhibited histamine-induced hyperemia compared to saline vehicle, while ranitidine and famotidine were not significantly inhibitory.
The results indicate that H1 receptors are solely responsible for histamine-mediated hyperemia and vascular permeability in the conjunctiva; H2 receptors play no part in these processes. It can be inferred from these data that the H2 receptor has no role in allergic conjunctivitis.
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