Coronary artery endothelial function after myocardial ischemia and reperfusion
| Autor: | Hartzell V. Schaff, John F. Seccombe |
|---|---|
| Rok vydání: | 1995 |
| Předmět: |
Pulmonary and Respiratory Medicine
medicine.medical_specialty Endothelium Receptors Peptide Ischemia Myocardial Ischemia Coronary Vasospasm Myocardial Reperfusion Myocardial Reperfusion Injury Nitric Oxide Nitric oxide Coronary circulation chemistry.chemical_compound GTP-Binding Proteins Internal medicine Coronary Circulation medicine Animals biology business.industry medicine.disease Coronary Vessels Nitric oxide synthase medicine.anatomical_structure chemistry Coronary vasospasm Cardiology biology.protein Surgery Artery Endothelium Amino Acid Oxidoreductases Endothelium Vascular Nitric Oxide Synthase Cardiology and Cardiovascular Medicine business Reactive Oxygen Species Reperfusion injury Signal Transduction |
| Zdroj: | The Annals of thoracic surgery. 60(3) |
| ISSN: | 0003-4975 |
| Popis: | Background. The consequences of ischemia-reperfusion injury on myocytes has been studied intensely, and previous investigations of methods of myocardial protection during global and regional ischemia have focused on resultant alterations in myocardial function. However, the coronary artery endothelium is also vulnerable to damage, and only recently have investigators been able to assess coronary endothelial function. Methods. This review examines some aspects of coronary flow abnormalities that occur after ischemia and reperfusion. In addition, we summarize recent data that address the hypothesis that injury to the coronary artery endothelium may contribute to the pathophysiology of global (and regional) cardiac ischemia and reperfusion. Results. It appears that ischemia and reperfusion selectively injure a component in the receptor/G-protein complex linking receptor-stimulus coupling to the activation of nitric oxide synthase. Further, oxygen radicals may contribute to this injury. Recent investigations demonstrate that oxygen radicals impair the receptor/G-protein complex specific to the nitric oxide signal transduction pathway rather than causing global receptor/G-protein dysfunction. Conclusions. The understanding of endothelial cell function and the elucidation of the nitric oxide pathway should further clarify our understanding of the pathogenesis of endothelial reperfusion injury and coronary vasospasm and contribute to the development of effective therapeutic interventions. |
| Databáze: | OpenAIRE |
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