Subject(s)
Epoprostenol/metabolism , Heart Arrest, Induced , Myocardium/metabolism , Prostaglandins/metabolism , 6-Ketoprostaglandin F1 alpha/analogs & derivatives , 6-Ketoprostaglandin F1 alpha/blood , Adult , Aged , Female , Humans , Lactates/metabolism , Lactic Acid , Male , Middle Aged , Oxygen ConsumptionABSTRACT
The pulmonary formation of prostacyclin (PGI2), as reflected by the difference in concentration of pulmonary and systemic arterial radioimmunoassayed 6-keto-PGF1 alpha, was determined in six healthy waking subjects. The systemic arterial 6-keto-PGF1 alpha levels were low (less than or equal to 50 pg/ml), and no evidence of pulmonary formation and release of the compound was noted. In other experiments systemic arterial 6-keto-PGF1 alpha levels were determined in patients prior to and during artificial ventilation, as well as during and after occlusion of the pulmonary circulation (extra-corporeal circulation, ECC). The arterial 6-keto-PGF1 alpha concentration prior to artificial ventilation was 17 +/- 4 pg/ml, i.e. within the range observed in the healthy subjects. During artificial ventilation the arterial levels of 6-keto-PGF1 alpha increased to 191 +/- 21 pg/ml, suggesting that pulmonary formation of PGI2 was stimulated. In the patients subjected to ECC with occluded pulmonary circulation the arterial content of 6-keto-PGF1 alpha was stabilised at an elevated level (120-170 pg/ml). Following re-establishment of the pulmonary circulation the arterial concentrations of 6-keto-PGF1 alpha increased markedly, to 284 +/- 50 pg/ml. It is suggested that the basal pulmonary formation of PGI2 in man is low or non-existent, and that enhanced formation of the compound in the lungs is a consequence of intervention with normal pulmonary ventilation of perfusion.
