1 When isolated perfused lungs from sensitized guinea-pigs were challenged with antigen, histamine, slow reacting substance of anaphylaxis (SRS-A) and prostaglandin-like substances were released into the effluent. 2 Treatment of the lungs before and during challenge with indomethacin (0.5-10 ig/ml), sodium aspirin (1-10 pg/ml), sodium meclofenamate (0.1-1 Mg/ml) or ketoprofen (0.5-5 /g/ml) inhibited the release of prostaglandins while increasing the output of histamine and SRS-A between threeand five-fold. 3 Diethylcarbamazine (0.2-1 mg/ml) reduced the release of SRS-A and histamine but increased the amount of prostaglandin-like substances produced. 4 Eicosatetraynoic acid (10 pg/ml) inhibited formation of prostaglandins but did not modify release of histamine and SRS-A. 5 The results with non-steroid anti-inflammatory drugs and diethylcarbamazine suggest that prostaglandins, or some other product of the cyclo-oxygenase system, depress the anaphylactic release of SRS-A and histamine.

(1976). Thorax, 31,[713][714][715][716][717][718][719]. Degradation of prostaglandin F,a in the human pulmonary circulation. Degradation of prostaglandins (PGs) during passage through the human pulmonary circulation was investigated by measuring the transpulmonary plasma PGF2a difference during continuous intravenous infusion of PGF2a (5-10 ,ug/min). Seven patients with cardiological disorders and two patients with extensive pulmonary abnormalities were investigated during diagnostic cardiac catheterization. PGF2a levels were measured by radioimmunoassay. The seven cardiac patients were found to have transpulmonary PGF2a differences of 47-88%, indicating metabolism of the PG in the lungs. A patient with extensive bronchiectasis had an apparently normal transpulmonary PGF2a difference despite gross abnormalities in routine lung function tests. A patient with primary pulmonary arterial hypertension showed no metabolism of PGF2a in the pulmonary circulation. The results show that PG degradation is an aspect of normal lung function and suggest that it becomes impaired when extensive pulmonary vascular damage exists.

No abstract

No abstract