Vascular permeability responses and the role of prostaglandin E₂ in an experimental allergic inflammation of air pouch type in rats

Abstract

1 Rats were sensitized with azobenzene arsonate-conjugated acetyl bovine serum albumin. An allergic inflammation was induced in the preformed air pouch in the dorsum of the sensitized rats by injecting the antigen dissolved in a 2% sodium carboxymethyl cellulose solution into the air pouch. 2 Time course changes of vascular permeability, accumulated pouch fluid volume and prostaglandin E2 (PGE2) levels in the pouch fluid were compared in sensitized and non-sensitized rats to characterize the allergic inflammatory reaction. 3 Effects of three cyclo-oxygenase inhibitors (indomethacin, diclofenac sodium and tiaprofenic acid) on vascular permeability and accumulated pouch fluid volume 4 and 24 h after the immunological challenge injection were examined to elucidate a possible role of PGE2 in the inflammatory response. 4 Four h after initiating the allergic reaction, although the level of PGE2 in the pouch fluid reached a high level, the vascular permeability response, measured over the period 3.5-4 h, was not suppressed by treatment with the three cyclo-oxygenase inhibitors and neither was the pouch fluid volume measured over the period 0-4 h. However, vascular permeability and accumulated pouch fluid volume at 24 h were suppressed by the cyclo-oxygenase inhibitors in a dose-dependent manner. 5 These observations suggest that in this model, endogenous PGE2 does not affect oedema formation measured at 4 h. However, oedema formation measured at 24 h may be dependent on PGE2 generation.

Mechanism of Antianaphylactic Action of β-Agonists in Allergic Inflammation of Air Pouch Type in Rats

“…Employing this model, which has ad vantages for biochemical and pharmacological analy sis of allergic inflammatory processes [18][19][20][21][22][23][24][25], the present study was intended to clarify whether the in vivo suppression by /(-agonists of the anaphylactic in crease in vascular permeability is brought about at the level of histamine release from mast cells or on the level of the local vascular system itself. and anti-rat IgG2a (c) solutions into the air pouch, a Sensitized rats ( + ) and nonsensitized rats (-) were injected with 4 ml of the antigen solution, b and c Intact rats were injected with 4 ml of a solution con taining anti-rat IgE or anti-rat !gG2a, re spectively.…”

Platelet-Activating Factor in the Inflammatory Exudate in the Anaphylactic Phase of Allergic Inflammation in Rats

“…The present work was intended to elucidate the physiologic significance of PAF in modulating acute allergic inflammation, by measuring the amount of PAF in the locus of inflammatory lesion in an experi mental model of allergic air pouch inflammation in rats [23,24], In this model, by injecting the antigen so lution into the air pouch, IgE-mediated anaphylactic increase of vascular permeability is induced within 30 min after the injection [25,26,32,33].…”

“…In an experimental model of allergic inflammation of air pouch type in rats, which has been devised in our laboratory [23,24], anaphylactic increase of vas cular permeability is induced [25,26] by injecting the antigen solution into the preformed air pouch on the dorsum. The present paper was undertaken to ex amine whether PAF is synthesized in the locus of the inflammatory site in this anaphylactic phase of the allergic inflammation, in order to get further insight into the physiological role of PAF in the anaphylactic reaction.…”

Possible roles of protein kinases in neutrophil chemotactic factor production by leucocytes in allergic inflammation in rats

“…During the course of experiments to identify the difference between allergic and non-allergic inflammation employing an air pouch-type inflammation model in rats 1985;Tsurufuji et al, 1982;Hirasawa et al, 1986;Watanabe et al,1987;1990), focused especially on the qualitative difference in the function of infiltrated leucocytes, we found (Watanabe et al, 1994) that the leucocytes ' Author for correspondence. infiltrated into the pouch fluid in the allergic inflammation model are much more active than those in the non-allergic inflammation model with respect to neutrophil chemotactic factor production.…”