Nasal congestion model in Brown Norway rats and the effects of some H1-antagonists

Tsumuro, Tae; Hossen, Maria Alejandra; Kishi, Yuko; Fujii, Yoko; Kamei, Chiaki

doi:10.1016/j.intimp.2005.11.009

Cited by 15 publications

(18 citation statements)

References 19 publications

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“…Almost the identical findings were already reported by ours. 8,9) In other words, an increase in Penh observed after TDI challenge was reconfirmed even in the present study. It was found that 17-phenyl trinor PGE 2 and butaprost had no significant effect on an increase of Penh in early phase after TDI challenge in sensitized rats.…”

Section: Discussionsupporting

confidence: 81%

Section: Methodsmentioning

confidence: 99%

“…Sensitization and Challenge Procedures Sensitization and challenge were performed according to the method described by Tsumuro et al 9) In brief, rats were sensitized by intranasal application of 10% TDI solution in ethyl acetate once a day for 5 consecutive days. Two days later, the rats were sensitized with TDI again for 5 d. One week after completion of the bilateral sensitization, 5% TDI solution in ethyl acetate was applied to the nasal cavities to induce nasal allergy-like symptoms.…”

Section: Methodsmentioning

confidence: 99%

“…TDI was dissolved in ethyl acetate to a concentration of 10% for sensitization and to a concentration of 5% for challenge. 17-Phenyl trinor PGE 2 , butaprost, sulprostone and PGE 1 alcohol were dissolved in saline and administered intravenously 10 min before antigen application.Sensitization and Challenge Procedures Sensitization and challenge were performed according to the method described by Tsumuro et al 9) In brief, rats were sensitized by intranasal application of 10% TDI solution in ethyl acetate …”

mentioning

confidence: 99%

“…[6][7][8] In an animal model, we have reported that although H 1 receptor antagonists inhibited the increase of enhanced pause (Penh) in early phase induced by toluene 2,4-diisocyanate (TDI) challenge, 9) a relatively high dose was needed. On the other hand, we reported that cys-LTs receptor antagonists (pranlukast, zafirlukast) and thromboxane A 2 (TXA 2 ) receptor antagonists (seratrodast, ramatroban) also caused an inhibitory effect on the increase of Penh in early and late phases after TDI challenge in sensitized rats.…”

mentioning

confidence: 99%

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Participation of Prostaglandin E2 Receptor in Nasal Congestion of Brown Norway Rats

Kurata

Yamamoto

Izawa

et al. 2010

Biological & Pharmaceutical Bulletin

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It is well known that histamine, cysteinyl leukotriene (cysLTs), thromboxanes, prostaglandins (PGs) and cytokines are responsible for allergic rhinitis. 1,2) There are two phases of allergic rhinitis response, named "early phase" and "late phase." Early phase response occurs within minutes of exposure to the allergen and is characterized by sneezing, rhinorrhea and nasal congestion. Late phase response occurs 4 to 8 h after allergen exposure and is characterized mainly by nasal congestion. 3)Histamine H 1 receptor antagonists, such as chlorpheniramine and astemizol, are widely used to treat allergic rhinitis clinically, 4,5) however, these H 1 receptor antagonists are not completely effective for nasal congestion. [6][7][8] In an animal model, we have reported that although H 1 receptor antagonists inhibited the increase of enhanced pause (Penh) in early phase induced by toluene 2,4-diisocyanate (TDI) challenge, 9) a relatively high dose was needed. On the other hand, we reported that cys-LTs receptor antagonists (pranlukast, zafirlukast) and thromboxane A 2 (TXA 2 ) receptor antagonists (seratrodast, ramatroban) also caused an inhibitory effect on the increase of Penh in early and late phases after TDI challenge in sensitized rats. 10) Therefore, it seems likely that different mediator is involved in early and late phase responses in nasal congestion.Prostaglandin E 2 (PGE 2 ) is arachidonic acid metabolite similar to LTs and TXA 2 , and there are four different receptors designated EP 1 , EP 2 , EP 3 and EP 4 . Kunikata et al. 10) reported that mice lacking EP 3 receptor developed potent allergic inflammation compared with wild-type mice or mice deficient in other prostaglandin E 2 receptor subtypes. On the other hand, Gomi et al.11) described that PGE 2 selectively enhanced the immunoglobulin E (IgE)-mediated production of interleukin-6 (IL-6). These actions may produce by the receptors other than EP 3 receptor.In a previous study, we established a nasal congestion model using Brown Norway (BN) rats by intranasal immunization with toluene 2,4-diisocyanate (TDI) as an antigen. 8)In this model, the animals showed not only sneezing but also nasal congestion in the early and late phases.In the present study, in order to clarify the role of PGE 2 receptor (EP 1 , EP 2 , EP 3 and EP 4 ) in the development of allergic rhinitis symptoms, we investigated the effects of each PGE 2 receptor agonists with a nasal congestion model in BN rats. MATERIALS AND METHODSAnimals Six-week-old male BN rats were obtained from Kyudo Co., Ltd. (Saga, Japan). The animals were housed in an air-conditioned room, maintained at 24Ϯ2°C, with relative humidity of 55Ϯ10%. The rats were given standard laboratory rodent food (Oriental Yeast, Tokyo, Japan) and water ad libitum. All procedures involving animals were conducted in accordance with the Guidelines for Animal Experiments at Okayama University Advanced Science Research Center.Materials The following reagents were obtained from the sources shown in parentheses: TDI (Wako, Tokyo, Japan)...

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Section: Discussionsupporting

confidence: 81%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 3 more Smart Citations

Participation of Prostaglandin E2 Receptor in Nasal Congestion of Brown Norway Rats

Kurata

Yamamoto

Izawa

et al. 2010

Biological & Pharmaceutical Bulletin

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Allergic Asthma and Rhinitis: Toxicological Considerations

Regal¹

2009

General, Applied and Systems Toxicology

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Immunotoxicity can manifest as an exaggerated immune response to a normally innocuous substance and lead to hypersensitivity or allergic reactions in the lung. Allergens are encountered environmentally or in the workplace and can be low‐ and high‐molecular‐weight substances. Allergic asthma and allergic rhinitis are examples of allergic reactions in the lung with immediate, late and chronic phases contributing to respiratory tract pathology. Mechanistically, allergic asthma and rhinitis reflect a combination of antibody and cell‐mediated immune reactions involving IgE antibody to allergen in the early stages and Th2 cell involvement as the disease progresses to late‐phase reactions and chronic allergic inflammation. Multiple cell types and mediators are involved in the inflammatory response in the lung. Mechanistic differences leading to the asthma/rhinitis phenotype have been noted with different allergens, primarily low‐molecular‐weight substances. Xenobiotics that are not allergens themselves may enhance the immune response to allergens or exacerbate pre‐existing asthma and airway hyper‐responsiveness. The complexity of the allergic response in terms of humoral and cell‐mediated immunity, as well as potential differences in mechanisms depending on the allergen, present a very challenging scenario for the toxicologist to predict the exposures that will result in allergic rhinitis or asthma.

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Airway responsiveness measured by barometric plethysmography in guinea pigs

et al. 2010

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Barometric plethysmography has become an increasingly used method to indirectly measure respiratory function in unrestrained freely-moving animals. This technique has been criticized because of physiological uncertainty of its major index, the enhanced pause (Penh). Moreover, a recent study raises concerns that during histamine challenges part of the Penh response could be produced by upper airways (nasal) responses. In this study we compared airway responsiveness measured by barometric plethysmography and total lung resistance (RL: ) in guinea pigs, and evaluated the role of upper airways during Penh measurement. Our results showed that intravenous acetylcholine or histamine caused a dose-dependent increase of the Penh values in non-anesthetized guinea pigs, which were correlated with RL: values obtained in separate groups of anesthetized animals. In anesthetized but spontaneously breathing guinea pigs intravenous acetylcholine or histamine also produced a dose-dependent increment of Penh, which was similar regardless if guinea pigs breathed through the nose or through a tracheal tube. Our results suggest that, independently of the physiological meaning of Penh, this index seems to be a useful indirect measurement for evaluating airway responsiveness to intravenous agonists in guinea pigs, and that nasal passage seems not to be involved in this measurement.

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Nasal congestion model in Brown Norway rats and the effects of some H1-antagonists

Cited by 15 publications

References 19 publications

Participation of Prostaglandin E2 Receptor in Nasal Congestion of Brown Norway Rats

Participation of Prostaglandin E2 Receptor in Nasal Congestion of Brown Norway Rats

Allergic Asthma and Rhinitis: Toxicological Considerations

Airway responsiveness measured by barometric plethysmography in guinea pigs

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