Endothelium bound extracellular superoxide dismutase type C reduces damage in reperfused ischaemic rat hearts
| Autor: | Per-Ove Sjöquist, Stefan L. Marklund |
|---|---|
| Rok vydání: | 1992 |
| Předmět: |
Male
medicine.medical_specialty Endothelium Physiology Ischemia Myocardial Reperfusion Injury Pharmacology Superoxide dismutase Reperfusion therapy Physiology (medical) Internal medicine medicine Animals Creatine Kinase chemistry.chemical_classification biology business.industry Superoxide Dismutase Rats Inbred Strains Heparin medicine.disease Rats Disease Models Animal medicine.anatomical_structure Enzyme chemistry Regional Blood Flow biology.protein Cardiology Creatine kinase Endothelium Vascular Cardiology and Cardiovascular Medicine business Extracellular Space Perfusion medicine.drug |
| Zdroj: | Cardiovascular research. 26(4) |
| ISSN: | 0008-6363 |
| Popis: | Objective: The aim was to determine if endothelium associated extracellular superoxide dismutase type C (EC-SOD C) exerts any protective effect against cardiac damage induced by ischaemia and reperfusion. Methods: Langendorff perfused rat hearts were subjected to 15 min global ischaemia followed by reperfusion. Prior to the ischaemia the hearts were perfused for 15 min with a buffer containing recombinant human EC-SOD C (rh-EC-SOD C, 20 mg·litre−1), or the corresponding vehicle, followed by extensive perfusion with SOD free medium. Results: In hearts receiving the vehicle, reperfusion was associated with a marked release of creatine kinase into the effluent [28 (SEM 1.5) IU·15 min−1, n=5] and coronary flow measured 15 min after initiation of reperfusion was reduced by 68% compared to preischaemic flow. In hearts pretreated with EC-SOD C but washed with enzyme free buffer before being subjected to ischaemia, the creatine kinase release was significantly smaller, at 14(2.1) IUmin−1, n=5 (p |
| Databáze: | OpenAIRE |
| Externí odkaz: |
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