Alterations in prostacyclin and thromboxane formation by chronic cigarette smoke exposure: Temporal relationships and whole smokevs. gas phase
| Autor: | William C. Lubawy, B. T. Culpepper, Monica A. Valentovic |
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| Rok vydání: | 1986 |
| Předmět: |
Male
Nicotine medicine.medical_specialty Thromboxane Prostacyclin 6-Ketoprostaglandin F1 alpha Toxicology chemistry.chemical_compound Smoke Internal medicine medicine.artery Tobacco medicine Animals Platelet Aorta Inhalation Thromboxanes Rats Inbred Strains Environmental Exposure Epoprostenol Rats Plants Toxic Endocrinology Carboxyhemoglobin chemistry Female lipids (amino acids peptides and proteins) Arachidonic acid medicine.drug |
| Zdroj: | Journal of Applied Toxicology. 6:77-80 |
| ISSN: | 1099-1263 0260-437X |
| DOI: | 10.1002/jat.2550060202 |
| Popis: | Chronic cigarette smoke exposure in vivo causes decreased conversion of [14C]arachidonic acid (AA) to prostacyclin (PGI2) by isolated aortic tissue and increased conversion to thromboxane (TXA2) by isolated platelets from rats. Alterations in the PGI2/TXA2 balance may be part of the mechanism through which smoking increases the risk of cardiovascular disease. To study the influence of smoke exposure duration on this response, male rats were exposed daily to 10 puffs of freshly generated cigarette smoke. Animals were klledd after 1, 4, 14, 28 and 57 days of smoke exposure and 3, 7, 14 and 28 days after cessation of the 57-day of smoke-exposure regimen. Elevated carboxyhemoglobin levels during the smoke-exposure sessions verified smoke (gas phase) inhalation. Statistically significant alterations in prostacyclin synthesis preceded those of thromboxane. A decrease of 20-25% (P |
| Databáze: | OpenAIRE |
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