Experimental myocardial infarction in a closed-chest canine model. Observations of temporal and spatial evolution over 24 hours.
Myocardial infarction was induced in 7 mongrel dogs by transfemoral intraluminal occlusion of the left anterior descending coronary artery. Perfusion area at risk was determined by post-mortem coronarography and infarct size by macrohistological staining with para-nitrophenoltetrazolium. Regional flow was determined by injection of radioactive microspheres 0.2 hours, 12 hours, and 24 hours post occlusion. Infarct size as determined by planimetry of post-mortem angiograms and macrohistological stains at identical magnification revealed 74.5 +/- 12.1% infarcted tissue of the perfusion area at risk. The flow of the necrotic tissue was below 13 Ml/100 g min without exception, indicating a threshold perfusion for maintenance of myocardial viability. Accordingly, a flow of less than or equal to 10 ml/100 g min identified 93% of the entire infarcted myocardium, resulting in 71 +/0 20% as compared to the perfusion area at risk. Based on the good agreement of macrohistological and flow data, the evolution of myocardial injury was determined by flow measurements. The results indicated a different progression of the borders of critical flow in the subendocardial and subepicardial layers, whereas in the subendocardium 85% of the tissue at risk was identified by the critical flow at 0.2 hours and 97% at 12 hours, the subepicardial flow changed at a different pace: only 53% showed subcritical perfusion at 0.2 hours, 61% at 12 hours with a final increase of 39% from 12 to 24 hours.
D000818:Animals; D003326:Coronary Circulation; D004285:Dogs; D004699:Endocardium / Q000473:pathology; D005260:Female; D008297:Male; D009203:Myocardial Infarction / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology