Prostacyclin and Thromboxane Production by Irradiated Rat Lung
| Autor: | J. M. Hinz, W. F. Ward |
|---|---|
| Rok vydání: | 1987 |
| Předmět: |
medicine.medical_specialty
Lung medicine.diagnostic_test biology Chemistry Thromboxane Captopril Prostacyclin Thromboxane Production chemistry.chemical_compound Bronchoalveolar lavage medicine.anatomical_structure Endocrinology Enzyme inhibitor Internal medicine medicine biology.protein lipids (amino acids peptides and proteins) Arachidonic acid circulatory and respiratory physiology medicine.drug |
| Zdroj: | Prostaglandin and Lipid Metabolism in Radiation Injury ISBN: 9781468454598 |
| DOI: | 10.1007/978-1-4684-5457-4_16 |
| Popis: | The production of prostacyclin (PGI2) and thromboxane (TXA2) by irradiated rat lung and the concentration of these prostanoids in the bronchoalveolar lavage (BAL) fluid were measured in rats sacrificed at 2 or 6 months after a single dose of 10-30 Gy of cobalt-60 gamma rays to the right hemithorax. Lung PGI2 and TXA2 production increased linearly with increasing radiation dose at rates of 3.1% and 4.3% per Gy, respectively, at 2 months and 21.7% and 6.1% per Gy, respectively, at 6 months. At both times, PGI2 and TXA2 production tended to plateau at doses of 25 Gy or higher. This plateau usually disappeared in the presence of exogenous arachidonic acid, suggesting that the Vmax for PGI2 production at 2 and 6 months and for TXA2 at 6 months was substrate-limited rather than enzyme-limited. At 2 months after irradiation, the modifying agents D-penicillamine (an inhibitor of collagen cross-linking) and Captopril (an angiotensin-converting enzyme inhibitor) exhibited significant dose-reduction factors of 1.3-1.8 for PGI2 production and 1.3-1.4 for TXA2 production. In the shielded left lung, PGI2 production increased slightly but significantly with increasing contralateral dose at 2 months postirradiation. The concentration of TXA2 in the BAL fluid increased linearly with increasing radiation dose at 2 months after exposure, whereas PGI2 concentration was independent of dose. At 6 months, the reverse was true. These data demonstrate that hemithorax irradiation produces a dose-dependent increase in pulmonary PGI2 and TXA2 production for at least 6 months, and suggest that BAL data may serve as an index of radiation-induced pulmonary damage. |
| Databáze: | OpenAIRE |
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