التفاصيل البيبلوغرافية
| العنوان: |
Oxidative stress and release of tissue plasminogen activator in isolated rat hearts |
| المؤلفون: |
Guro Valen, Jarle Vaage, Björn Wiman, Anders Winnerkvist |
| المصدر: |
Thrombosis research. 85(3) |
| سنة النشر: |
1997 |
| مصطلحات موضوعية: |
Male, medicine.medical_specialty, Endothelium, Bradykinin, In Vitro Techniques, medicine.disease_cause, Tissue plasminogen activator, Ventricular Function, Left, Rats, Sprague-Dawley, chemistry.chemical_compound, Heart Rate, Internal medicine, Lactate dehydrogenase, medicine, Animals, Hydrogen peroxide, L-Lactate Dehydrogenase, T-plasminogen activator, Chemistry, Myocardium, Plasminogen, Hematology, Hydrogen Peroxide, Rats, Oxidative Stress, Endocrinology, medicine.anatomical_structure, Biochemistry, Perfusion, Oxidative stress, medicine.drug |
| الوصف: |
To evaluate the potential of tissue plasminogen activator (t-PA) as a marker of endothelial activation or injury, the dose-response relationship between reactive oxygen intermediates and t-PA release was investigated in isolated rat hearts. After stabilization the hearts were perfused for 10 minutes with different concentrations of hydrogen peroxide (H 2 O 2 ) (0 (control perfusion), 20, 40, 80, 120, 160, or 200 μM) (n=8 hearts/group), followed by 30 minutes recovery. Higher concentrations than 80 μM induced cardiac dysfunction and a dose-dependent release of lactate dehydrogenase, indicating myocyte injury. H 2 O 2 -concentrations of 80 μM and more caused a significant, but temporary t-PA release. Peak t-PA release occurred more rapidly with higher concentrations, but otherwise there was no difference dependent on the H 2 O 2 -dose. The effects of H 2 O 2 (120 or 200 μM) on t-PA release were also compared to the effects of bradykinin. Both were given for 10 minutes as above, and the procedure was repeated after 10 minutes recovery. Bradykinin (50 or 500 nM) released t-PA with the same magnitude, but with peak values occurring earlier than t-PA release induced by H 2 O 2 . Bradykinin, but not H 2 O 2 , induced t-PA release during the second exposure, suggesting different mechanisms of release. In conclusion: Perfusion with H 2 O 2 leads to a dose-dependent myocardial injury in isolated rat hearts. H 2 O 2 also causes an acute t-PA release without dose-dependency, suggesting an all or nothing response of the endothelium. t-PA may be used as an indicator of, but cannot quantify endothelial activation or injury. Copyright © 1997 Elsevier Science Ltd |
| تدمد: |
0049-3848 |
| الوصول الحر: |
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::df32f8ba99a98e20931cc621c32fd0eaTest
https://pubmed.ncbi.nlm.nih.gov/9058499Test |
| حقوق: |
CLOSED |
| رقم الانضمام: |
edsair.doi.dedup.....df32f8ba99a98e20931cc621c32fd0ea |
| قاعدة البيانات: |
OpenAIRE |
