Pulmonary formation of prostacyclin in man
Autor: | E. Pinca, A. Edlund, W. Bomfim, Carlo Patrono, Åke Wennmalm, Lennart Kaijser, C. Olin |
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Rok vydání: | 1981 |
Předmět: |
Adult
Male Artificial ventilation medicine.medical_treatment Radioimmunoassay Prostacyclin 6-Ketoprostaglandin F1 alpha Biochemistry Basal (phylogenetics) Endocrinology Occlusion Humans Medicine In patient Cardiac Surgical Procedures Lung Aged business.industry Middle Aged Epoprostenol Respiration Artificial medicine.anatomical_structure Anesthesia Prostaglandins Female lipids (amino acids peptides and proteins) business Perfusion medicine.drug |
Zdroj: | Prostaglandins. 22:323-332 |
ISSN: | 0090-6980 |
DOI: | 10.1016/0090-6980(81)90046-0 |
Popis: | 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. |
Databáze: | OpenAIRE |
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