Plasma Prostaglandin Concentrations in Allergic Bronchial Asthma

Okazaki, Tadao; Johnson, Thomas F.; Reisman, Robert E.; Arbesman, Carl E.; Middleton, Elliott

doi:10.1159/000232114

Cited by 3 publications

(2 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[5], Dry et al [6) and Buisseret et al (4), who all used the same method (5). Other authors (1,23,25), how ever, showed considerably higher values which differ to a large extent. This is cer tainly due to the sampling conditions: lack of aspirin in the sampling medium (1,8,24], release of PG during the coagulation when the determinations are carried out on scrum [23; table III).…”

Section: Discussionmentioning

confidence: 79%

See 1 more Smart Citation

Plasma Concentrations of Prostaglandins E2 and F2α in Asthmatic Patients

Godard¹,

Chantreuil

Clauzel³

et al. 1981

Respiration

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

confidence: 79%

“…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 E2 and F2α in Asthmatic Patients

Godard¹,

Chantreuil

Clauzel³

et al. 1981

Respiration

View full text Add to dashboard Cite

show abstract

Comparison of histamine release and prostaglandin E2 production of human basophils in atopic and normal individuals

1987

View full text Add to dashboard Cite

The influence of arachidonic acid (AA) metabolism upon histamine release (HR) from human basophils after stimulation with anti-IgE was studied in 23 atopic and 11 normal individuals. HR occurred significantly faster in atopics than in normals; the total amount of HR after a 40 min incubation period was not significantly different between the two groups. Indomethacin and acetylsalicylic acid (ASA) increased the quantity of HR significantly both in atopics and normals without influencing the time course. Addition of exogenous PGE2 decreased HR; here atopics were more affected than normals 5 and 10 min after challenge with anti-IgE. Production of PGE2 after stimulation with anti-IgE was very low in both groups (in the range of 30-50 pg/10(6) cells) and often below detection limit (10-20 pg/ml). Addition of glutathione (GSH), a coenzyme of PGE2-isomerase, increased PGE2 production 2 to 5-fold during stimulation with anti-IgE. These data support the idea that arachidonic acid metabolites play an important role in modulating the "releasability" of human basophils. It is suggested that the basophils of atopic individuals may release their histamine faster than normals - perhaps on the basis of a more slowly acting endogenous feedback mechanism by PGE2. Both phenomena support the idea of an altered "releasability" of basophils from atopics compared to normals.

show abstract

Allergen tachyphylaxis of guinea pigs in vivo: A prostaglandin E mediated phenomenon?

Dorsch¹,

Frey²

1981

Naunyn-Schmiedeberg's Arch. Pharmacol.

View full text Add to dashboard Cite

Ovalbumin (OA) sensitized guinea pigs were repeatedly challenged with 1% OA in saline nebulized ultrasonically at the 0, 10, 20, 60 and 70th min. The intensity of bronchial obstruction was measured by body plethysmography. The first three challenges (0. 10, 20 min) caused strong asthmatic reactions in all animals, the last two (60, 70 min) only mild one in 10 out of 15 animals. The development of this "tachyphylaxis" was markedly reduced by pretreatment of the animals with cyclooxygenase inhibitors (indomethacin 10 mg/kg intraperitoneally resp, acetylsalicylic acid 10 mg/kg orally 2 h before tests). The effect of both inhibitors (i.e. inhibition of tachyphylaxis) was abolished by supplementing prostaglandin E2 as aerosol simultaneously to the allergen (100-200 ng per inhalation). The results suggest that allergen tachyphylaxis we have observed in vivo might be due to synthesis of cyclooxygenase products, e.g. prostaglandin E.

show abstract

Plasma Prostaglandin Concentrations in Allergic Bronchial Asthma

Cited by 3 publications

References 8 publications

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

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

Comparison of histamine release and prostaglandin E2 production of human basophils in atopic and normal individuals

Allergen tachyphylaxis of guinea pigs in vivo: A prostaglandin E mediated phenomenon?

Contact Info

Product

Resources

About