Neutrophil superoxide anion generation during atorvastatin and fluvastatin therapy used in coronary heart disease primary prevention
| Autor: | Maciej Banach, Robert Irzmański, Lucjan Pawlicki, Joanna Grycewicz, Marcin Barylski, Jan Kowalski |
|---|---|
| Rok vydání: | 2006 |
| Předmět: |
Drug
Adult Male Indoles Neutrophils media_common.quotation_subject Atorvastatin Coronary Disease Pharmacology Superoxide dismutase Fatty Acids Monounsaturated chemistry.chemical_compound Superoxides medicine Humans Pyrroles Vein Fluvastatin media_common Whole blood biology business.industry Superoxide Zymosan Middle Aged Lipoproteins LDL Primary Prevention medicine.anatomical_structure chemistry Heptanoic Acids biology.protein Female Hydroxymethylglutaryl-CoA Reductase Inhibitors Cardiology and Cardiovascular Medicine business medicine.drug |
| Zdroj: | Journal of cardiovascular pharmacology. 48(4) |
| ISSN: | 0160-2446 |
| Popis: | Neutrophil superoxide anion generation was measured during atorvastatin and fluvastatin therapy in patients with coronary heart disease (CHD) risk. The patients were randomly allotted into three groups. The atorvastatin group comprised 17 patients who were administered the drug orally 10 mg a day at bed time. The fluvastatin group consisted of 18 patients on an oral dose of 40 mg once daily at bed time. The control group comprised 12 healthy subjects with no drug administration. Blood samples were collected from cubital vein before and after 6-week therapy with these drugs and once in the control group. Neutrophil superoxide anion generation in whole blood without and with opsonized zymosan (OZ) stimulation was determined using superoxide dismutase from bovine erythrocytes. In the atorvastatin group, statistically significant (P < 0.05) decrease in superoxide anion generation by nonstimulated and OZ-stimulated neutrophils was observed after 6 weeks of therapy. In fluvastatin group, no changes in neutrophil superoxide anion generation were observed after the 6-week treatment period. Our study has shown an additional nonlipid mechanism of atorvastatin used in CHD primary prevention. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|