Further Studies on Passive Peritoneal Anaphylaxis in the Rat

Abstract

Four compounds with H₁ anti-histamine activity and four adrenoceptor stimulants, each given to rats prior to passive peritoneal anaphylaxis (PPA), inhibited extravasation of serum proteins into the peritoneal fluid at doses which had no effect on histamine release. In contrast, aminophylline and some non-steroidal anti-inflammatory agents inhibited extravasation only at doses which inhibited histamine release; they showed a similar type of activity to that of disodium cromoglycate (DSCG) and a nitroindanedione (BRL 10833), although they were much less potent. Predosing with DSCG reduced the potency of subsequent doses of DSCG, BRL 10833 and indomethacin, but not of aminophylline or phenylbutazone, and therefore DSCG, BRL 10833 and indomethacin may share a common pathway to produce activity. In the rat PPA system, no evidence was found for histamine ‘feedback’ inhibition of histamine release.

The Effects of the Immunologic Release of Histamine upon Human Lung Cyclic Nucleotide Levels and Prostaglandin Generation

“…Histamine may have a cyclic AMP-dependent (13), H-2-mediated (40) autoinhibitory capacity in regard to basophil leukocyte histamine release. This observation may, in part, be species specific, because histamine is capable of inhibition of SRS-A release from bovine lung (41) but fails to influence mediator release from the rat peritonium (42). Histamine H-2 receptor antagonists augment reversed anaphylactic histamine release from monkey skin (41) but not from rat lung (43).…”

Involvement of β-Adrenergic Systems in the Antagonizing Effect of Paeoniflorin on the Scopolamine-Induced Deficit in Radial Maze Performance in Rats

“…anaphylactic histamine release from human basophils is regulated by H2-receptors, the stimulation of which results in the inhibition of the release by elevation of the cellular levels of cyclic adenosine monophosphate (14,15). On the other hand, anaphylactic histamine release from rat peritoneal mast cells has been reported not to be influenced by an H2-antagonist, cimetidine, suggesting that H2-receptors are not involved in the regulation of anaphylactic histamine release in this cell (16,17).…”

Rat Passive Peritoneal Anaphylaxis Following Sensitisation with Guinea Pig Antiserum: an Immediate Hypersensitivity Reaction without Histamine Release

“…It contrasts with peritoneal anaphylaxis pro duced in rats after sensitisation with antise ra raised in rats or mice by IgE-directing schedules, in which histamine is the main mediator of the extravasation produced [21,24]. Extravasation, during PPA in rats sen sitised with guinea pig antiserum, was not reduced by prior treatment of the rats with the H, antihistamines pyrilamine and cy proheptadine [8], given at doses which pro duced a marked inhibition of extravasation in PPA produced in rats sensitised with rat antiserum [23], Methysergide, a 5-HT an tagonist [8], when given at high doses [22], also failed to inhibit extravasation of PPA in rats sensitised with guinea pig antiserum. Administration of high doses of the SRS-A antagonist FPL 55712 [1] or BRL 19880 [5] to rats, just before subjecting them to this type of PPA, had no effect on the extra vasation.…”

“…The /1-adrenoceptor stimulants were at least as potent as inhibitors of extravasation as of SRS-A release when given to rats just before subjecting them to PPA, after sensi tisation with guinea pig antiserum. The po tent inhibition of extravasation shown by these compounds is probably due to a direct effect on the vasculature, and they have been shown to be antagonists of the vascu lar permeability effects of histamine in the peritoneal cavity of the rat [23].…”