Antiallergic activity of 2-nitroindan-1,3-diones

When actively sensitised rats were injected intraperitoneally with antigen, the local reaction that ensued can be divided into two phases: an immediate reaction characterised by histamine and SRS-A release with an associated extravasation of plasma proteins, and a late reaction involving infiltration of neutrophilic polymorphonuclear leucocytes. When the immediate reaction was modified by BRL 10833 (which inhibits histamine release from rat mast cells and reduces extravasation of plasma proteins), there was no reduction in neutrophil infiltration. FPL 55712, an SRS-A antagonist, also failed to inhibit neutrophil infiltration. The β-adrenoreceptor stimulants isoprenaline and salbutamol reduced neutrophil infiltration. Isoprenaline inhibited the extravasation of plasma proteins when given before antigen, but even when administered to rats after antigen, when extravasation was complete, it still inhibited neutrophil infiltration. Propranolol reversed isoprenaline-induced inhibition of neutrophil infiltration.

Section: Compoundsmentioning

confidence: 99%

Effects of Drugs on the Acute Inflammation Following Intraperitoneal Injection of Antigen into Actively Sensitised Rats

Sharpe¹,

Smith²

1979

“…London, UK). Animals were sensitised with the grade III ovalbumin and rats were challenged with the grade V. [4,5]; phenidone (l-phenyl-3-pyrazolidone) and DL-isoproterenol sulfate (Sig ma, St. Louis, Mo. ); salbutamol (Allen & Hanbury, Ware, UK); Hetrazan (diethylcarbamazine; Lederle Lab., Pearl River, N.Y.).…”

Section: Animalsmentioning

confidence: 99%

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

Smith¹,

Ross²,

Spicer³

1980

Self Cite

Antigen challenge of rats, sensitised by an intraperitoneal injection of guinea pig antiserum, produced an antibody-dependent increase in concentrations, in the peritoneal fluids, of slow-reacting substance of anaphylaxis (SRS-A) and of extravasated, dye-labelled, plasma proteins but not of histamine or 5-hydroxytryptamine. The SRS-A released may not be the main mediator of the extravasation since pre-treatment of the rats with the SRS-A antagonists FPL 55712 and BRL 19880 had no effect on extravasation, and a number of compounds, given in a similar way, were more potent as inhibitors of SRS-A release than of extravasation. Rat passive peritoneal anaphylaxis (PPA), following sensitisation with guinea pig antiserum, provides an example of an immediate hypersensitivity reaction in which there is no antibody-dependent release of histamine and in which the SRS-A released may not mediate all of the extravasation produced.

“…Disodium cromoglycate (Fison's Pharmaceuticals, Loughborough, England); so dium nivimedone is BRL 10833, the sodium salt of 5,6-dimethyl-2-nitroindane-l,3-dione and was prepared in our laboratories [2].…”

Section: Antigenmentioning

confidence: 99%

Peritoneal Anaphylaxis in the Rat after Sensitisation with Mouse Antiserum

Spicer¹,

Ross²,

Sharpe³

et al. 1978

Self Cite

Passive peritoneal anaphylaxis in rats, sensitised with mouse antiserum, had characteristics of an IgE-mediated reaction, in that the serum was heat-labile and pretreatment of the rats with disodium cromoglycate (DSCG), or sodium nivimedone, inhibited the release of both histamine and slow-reacting substance of anaphylaxis (SRS-A). Sodium nivimedone was more potent than DSCG as an inhibitor of histamine release. Peak concentrations of histamine and SRS-A in the peritoneal fluids of the rats, were reached within 2 min of antigen challenge and fell to control levels after 20–30 min.