Coronary Artery Reperfusion
Open Access
- 1 October 1972
- journal article
- Published by American Society for Clinical Investigation in JCI Insight
- Vol. 51 (10), 2717-2723
- https://doi.org/10.1172/jci107091
Abstract
The question of whether or not the size of an area of myocardial infarction, measured at 1 wk after coronary occlusion, can be influenced by coronary artery reperfusion was examined in dogs. In seven control experiments the anterior descending coronary artery was ligated, while in seven other studies the occlusion was released after 3 hr. In all animals calibrated photographs were used to assess the zone of hypoperfusion and the acutely injured area of epicardial ST segment elevation, as well as the extent of damage at postmortem 1 wk later. In control dogs, the gross infarct size at postmortem averaged 63.8±7.3% of that predicted from the acutely injured zone. However, in reperfused hearts the average gross infarct size at 1 wk was only 10.2±4.4% of that predicted. Transmural specimens were obtained at autopsy for histology and measurement of myocardial creatine phosphokinase (CPK) activity from sites initially used for epicardial electrocardiography. In control animals, there was a direct relationship between the degree of ST segment elevation and the degree of cell necrosis in transmural histologic sections. ST segment elevation also predicted myocardial CPK (international units per milligram protein): log CPK = − 0.0613 ST + 1.17 (r = 0.66, n = 56 sites). In the reperfused animals, log CPK = − 0.166 ST + 1.36 (r = 0.69, n = 46 sites) showing almost complete preservation of CPK activity at 1 wk, sparing being most prominent in the epicardial zone. Similarly, there was a good correlation between myocardial CPK activity and the histological assessment of cell destruction, the degree of cell damage = − 0.152 CPK + 3.86 (r = 0.86; n = 102 sites). Thus, control dogs showed severe myocardial CPK depletion and histologic evidence of extensive cell destruction, whereas animals subjected to coronary artery reperfusion had little CPK depletion and much less evidence of myocardial cell necrosis 1 wk later.Keywords
This publication has 18 references indexed in Scilit:
- Coronary Artery ReperfusionJCI Insight, 1972
- Acute coronary insufficiency (impending myocardial infarction and myocardial infarction): Surgical treatment by the saphenous vein graft techniqueThe American Journal of Cardiology, 1971
- Depressed Myocardial Creatine Phosphokinase Activity Following Experimental Myocardial Infarction in RabbitCirculation Research, 1970
- Structural and functional abnormalities in mitochondria isolated from ischemic dog myocardium.1969
- The influence of diastolic augmentation on infarct size following coronary artery ligationThe Journal of Thoracic and Cardiovascular Surgery, 1967
- EXPERIMENTAL ACUTE MYOCARDIAL INFARCTION - HISTOLOGIC + HISTOCHEMICAL STUDIES OF EARLY MYOCARDIAL INFARCTS INDUCED BY TEMPORARY 3R PERMANENT OCCLUSION OF CORONARY ARTERY1964
- The extent of reversibility of myocardial ischemia in dogsAmerican Heart Journal, 1959
- MYOCARDIAL ISCHEMIA AND EARLY INFARCTION - AN ELECTRON MICROSCOPIC STUDY1959
- Oxygen Uptake of the Nonworking Left VentricleCirculation Research, 1958
- Ensymatic changes in acute myocardial ischemic injury; glutamic oxaloacetic transaminase, lactic dehydrogenase, and succinic dehydrogenase.1957