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British Journal of Pharmacology logoLink to British Journal of Pharmacology
. 1990 Mar;99(3):449–454. doi: 10.1111/j.1476-5381.1990.tb12948.x

Vasodilatation and inhibition of mediator release represent two distinct mechanisms for prostaglandin modulation of acute mast cell-dependent inflammation.

J Raud 1
PMCID: PMC1917358  PMID: 2158843

Abstract

1. Intravital microscopy of the hamster cheek pouch was used to examine the influence of vasodilator prostanoids (prostaglandin E2 (PGE2), PGI2), forskolin, and nitroprusside on the microvascular changes during acute inflammation induced by antigen or histamine. The results extend our previous finding that PGE2 modulates allergic inflammation and histamine release in the cheek pouch model. 2. The microvascular actions of arachidonic acid and different cyclo-oxygenase products (PGE2, PGD2, PGI2, PGF2 alpha, and the thromboxane A2 (TXA2)-analogue U-44069) were first compared with respect to their effects on arteriolar tone. Of the prostaglandins, only PGE2 and PGI2 were potent vasodilators and markedly increased local blood flow. Nitroprusside and forskolin also caused vasodilatation and increased blood flow, but were somewhat less potent than PGE2 and PGI2. 3. Topically applied PGE2 and PGI2 in vasodilator concentrations suppressed the antigen-induced plasma leakage. On the other hand, although the antigen response was predominantly mediated by histamine, both prostaglandins enhanced the plasma leakage evoked by exogenous histamine. 4. In contrast, the vasodilator nitroprusside, in a dose causing an increase in blood flow equal to that of PGE2 and PGI2, potentiated both the histamine-induced plasma leakage, as well as the plasma and leukocyte extravasation after antigen challenge, indicating that the anti-inflammatory actions of the prostaglandins were unrelated to their vasodilator properties per se.(ABSTRACT TRUNCATED AT 250 WORDS)

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Selected References

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