INCREASED PLASMA LEVELS OF 15-Keto- 13,14-Dihydro-Prostaglandin F2α AFTER ALLERGEN-PROVOKED ASTHMA IN MAN

Gréen, Krister; Hedqvist, Per; Svanborg, Nils

doi:10.1016/s0140-6736(74)90075-0

Cited by 100 publications

(21 citation statements)

References 14 publications

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“…Increased levels of metabolites of thromboxane A2 (TXA2) have been measured in the plasma and urine following antigen provocation in asthmatics (Green et al, 1974;Shepherd et al, 1985;Sladek et al, 1990) and increased prostaglandin D2 (PGD2) and TXA2 levels have been observed in bronchoalveolar lung fluid obtained following antigen challenge (Murray et al, 1986;Wenzel et al, 1989;Liu et al, 1990). …”

Section: Introductionmentioning

confidence: 99%

BAY u3405 an antagonist of thromboxane A₂‐ and prostaglandin D₂‐induced bronchoconstriction in the guinea‐pig

Francis

Greenham

Patel

et al. 1991

British J Pharmacology

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1 The novel thromboxane (TX) antagonist, BAY u3405, has been evaluated against bronchoconstriction induced by the TXA2 mimetic U-46619, prostaglandin D2 (PGD2), 5-hydroxytryptamine (5-HT), leukotriene D4 (LTD4) and histamine in the guinea-pig in vivo by use 6 The action of BAY u3405 (l0mgkg-,p.o.) was long lasting, causing significant inhibition of U-46619-induced bronchoconstriction 7 h after dosing. 7 At 1 mg kg-1, i.v., a dose that abolished the response to U-46619 and PGD2, BAY u3405 had no effect on histamine-, 5-HT-or LTD4-induced bronchoconstriction. 8 BAY u3405 potently and selectively antagonized U-46619-or PGD2-induced bronchoconstriction in the Konzett-Rbssler model of guinea-pig lung function. It should therefore prove to be a useful tool for defining the role of TXA2-and PGD2 in airway diseases such as asthma.

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Section: Introductionmentioning

confidence: 99%

BAY u3405 an antagonist of thromboxane A₂‐ and prostaglandin D₂‐induced bronchoconstriction in the guinea‐pig

Francis

Greenham

Patel

et al. 1991

British J Pharmacology

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“…in man (Mathe, Hedquist, Holmgren & Svanborg, 1973) there has been speculation about a possible role for prostaglandins in the pathogenesis of asthma. The release of prostaglandins by antigen-challenged human lung in vitro (Piper & Walker, 1973) and the presence of a prostaglandin F2a metabolite in the blood of asthmatic patients on inhalation of antigen (Green, Hedquist & Svanborg, 1974) (Vane, 1971), was investigated to establish whether this prostaglandin participates in the contraction of sensitized human bronchus when exposed to antigen in vitro.…”

Section: Introductionmentioning

confidence: 99%

REDUCTION OF ANTIGEN‐INDUCED CONTRACTION OF SENSITIZED HUMAN BRONCHUS in vitro BY INDOMETHACIN

Dunlop

Smith

1975

British J Pharmacology

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Contraction of passively sensitized human bronchus induced by antigen challenge in vitro, was reduced by the prostaglandin F2α synthetase inhibitor, indomethacin. Prostaglandin F2α was released during challenge and this release was inhibited by indomethacin. There was a significant correlation between prostaglandin F2α release and antigen challenge‐induced contraction, suggesting that this substance may contribute to the bronchoconstrictor response of sensitized human bronchus to antigen.

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“…Studies of circulating PGs in asthmatic patients are rare [1,6,8,11,[23][24][25], espe cially if we consider the great number of in vestigations carried out in vitro, in animals and man [16,20], which were always limit ed to the determination in systemic venous blood. PGs are 'local' hormones, mediators, i.e.…”

Section: Discussionmentioning

confidence: 99%

Plasma Concentrations of Prostaglandins E<sub>2</sub> and F<sub>2α</sub> in Asthmatic Patients

Godard¹,

Chantreuil

Clauzel³

et al. 1981

Respiration

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Plasma concentrations of prostaglandins E₂ (PGE₂) and F_2α (PGF_2α) are studied in venous and arterial blood in 14 healthy subjects and 32 asthmatic patients. In the asthmatic patients we found: (1) a good correlation between PGE₂ concentration in venous blood and the seriousness of the airway obstruction; (2) a good correlation between PGE₂ and PGF_2α in the arterial blood, but not in the venous blood; (3) a decrease in the arterial concentrations of PGE₂ and PGF_2α after fenoterol-induced bronchodilatation, but the variations of PGE₂ and PGF_2α still correlate. None of these results were obtained in normal subjects. It seems that the asthmatic allergic patient has a disorder of the metabolism of prostaglandins in the lungs; however, the results obtained do not allow us to say if it is a causal condition or a metabolic consequence of the bronchospasm. Concerning the venous blood, there could be an increase in the peripheral production of PGE₂ which might result from the hypoxemia following airway obstruction.

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INCREASED PLASMA LEVELS OF 15-Keto- 13,14-Dihydro-Prostaglandin F2α AFTER ALLERGEN-PROVOKED ASTHMA IN MAN

Cited by 100 publications

References 14 publications

BAY u3405 an antagonist of thromboxane A₂‐ and prostaglandin D₂‐induced bronchoconstriction in the guinea‐pig

BAY u3405 an antagonist of thromboxane A₂‐ and prostaglandin D₂‐induced bronchoconstriction in the guinea‐pig

REDUCTION OF ANTIGEN‐INDUCED CONTRACTION OF SENSITIZED HUMAN BRONCHUS in vitro BY INDOMETHACIN

Plasma Concentrations of Prostaglandins E<sub>2</sub> and F<sub>2α</sub> in Asthmatic Patients

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INCREASED PLASMA LEVELS OF 15-Keto- 13,14-Dihydro-Prostaglandin F2α AFTER ALLERGEN-PROVOKED ASTHMA IN MAN

Cited by 100 publications

References 14 publications

BAY u3405 an antagonist of thromboxane A2‐ and prostaglandin D2‐induced bronchoconstriction in the guinea‐pig

BAY u3405 an antagonist of thromboxane A2‐ and prostaglandin D2‐induced bronchoconstriction in the guinea‐pig

REDUCTION OF ANTIGEN‐INDUCED CONTRACTION OF SENSITIZED HUMAN BRONCHUS in vitro BY INDOMETHACIN

Plasma Concentrations of Prostaglandins E<sub>2</sub> and F<sub>2α</sub> in Asthmatic Patients

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Product

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BAY u3405 an antagonist of thromboxane A₂‐ and prostaglandin D₂‐induced bronchoconstriction in the guinea‐pig

BAY u3405 an antagonist of thromboxane A₂‐ and prostaglandin D₂‐induced bronchoconstriction in the guinea‐pig