Studies of the mechanisms involved in the fate of prostacyclin (PGI2) and 06-keto-PGF1α in the pulmonary circulation |
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| Authors: | Hollis J. Hawkins J.Bryan Smith Kyriacos C. Nicolaou Thomas E. Eling |
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| Affiliation: | 1. Prostaglandins Section Laboratory of Pulmonary Function and Toxicology National Institute of Environmental Health Sciences Research Triangle Park, North Carolina 27709 USA;2. Cardeza Foundation Thomas Jefferson University Philadelphia, Pennsylvania 19107 USA;3. Department of Chemistry University of Pennsylvania Philadelphia, Pennsylvania 19104 USA |
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| Abstract: | We have investigated the metabolism of [3]H-prostaglandin (PG)I2 and its non-enzymatic breakdown product [3]H-6-keto-PGF1α by rat pulmonary tissue and their possible uptake and metabolism upon passage through the isolated perfused rat lung. When incubated with rat lung homogenate in the presence of β-NAD, [3]H-PGI2 was extensively degraded into at least one metabolite, while [3]H-6-keto-PGF1α was only minimally metabolized. However, on passage through isolated perfused rat lungs, neither [3]H-PGI2 nor [3]H-6-keto-PGF1α were removed from the circulation into the lung or degraded. This demonstration that PGI2 is not a substrate for the transport system for the removal of PGs from the circulation into the lung further illustrates that this system is a critical determinant for the pulmonary inactivation of circulating prostaglandins. The experimental findings are discussed in reference to the structure-activity requirements necessary for pulmonary transport and subsequent metabolism. |
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