The wavefront phenomenon of ischemic cell death. 1. Myocardial infarct size vs duration of coronary occlusion in dogs
| Autor: | M M Rasmussen, Keith A. Reimer, Robert B. Jennings, James E. Lowe |
|---|---|
| Rok vydání: | 1977 |
| Předmět: |
medicine.medical_specialty
Time Factors Necrosis Cell Survival Myocardial Infarction Ischemia Hemodynamics Hemorrhage Electrocardiography Coronary circulation Dogs Coronary Circulation Physiology (medical) Internal medicine Occlusion medicine Animals Myocardial infarction Circumflex business.industry Myocardium Papillary Muscles medicine.disease Coronary Vessels Disease Models Animal medicine.anatomical_structure Coronary occlusion Anesthesia Cardiology medicine.symptom Cardiology and Cardiovascular Medicine business Endocardium |
| Zdroj: | Circulation. 56:786-794 |
| ISSN: | 1524-4539 0009-7322 |
| DOI: | 10.1161/01.cir.56.5.786 |
| Popis: | Irreversible ischemic myocardial cell injury developes in an increasing number of cells as the duration of coronary occlusion is prolonged. The present study quantitates myocardial necrosis produced by 40 minutes, 3 hours, or 6 hours of temporary circumflex coronary occlusion (CO) followed by 2 to 4 days of reperfusion, or by 24 or 96 hours of permanent circumflex ligation in pentobarbital anesthetized open chest dogs. After 40 minutes of ischemia, myocyte necrosis was subendocardial but with increasing duration of coronary occlusion, irreversible injury progressed as a wavefront toward the subepicardium. Transmural necrosis was 38 +/- 4% after 40 min, 57 +/- 7% after 3 hours, 71 +/- 7% after 6 hours and 85 +/- 2% after 24 hours of ischemic injury. These results document the presence of a subepicardial zone of ischemic but viable myocardium which is available for pharmacologic or surgical salvage for at least three and perhaps six hours following circumflex occlusion in the dog. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|