A nonflow basis for the vulnerability of the subendocardium.
The functional consequences of a transmural gradient of metabolism in the heart were studied in 19 dogs. The technique of retrograde blood flow diversion after coronary occlusion was used to deplete the ischemic myocardium of blood flow. Blood flow was uniformly and equally depleted in all layers, averaging 0.044 ml/min per g. With oxygen supply a controlled variable, transmural differences in metabolic demand can be addressed. In groups of dogs severe myocardial ischemia was induced for periods of 20 to 90 minutes. No necrosis was noted after 20 minutes of ischemia. Beginning at 30 minutes of blood flow depletion, necrosis progressed from the endocardium toward the epicardium in a "wave front" pattern. At 90 minutes of ischemia, approximately 70% of the area at risk was necrotic. Thus, the relative vulnerability of the endocardium as compared with the epicardium is due to nonflow factors, and probably dictated by transmural differences in metabolic activity. It would appear that myocardial metabolism as compared with blood flow occupies a primary and overriding role during the first 20 minutes of ischemia. Furthermore, differences in transmural metabolism also dictate subendocardial vulnerability for ischemic periods greater than 20 minutes, irrespective of blood flow. The role of blood flow in these events may be to modulate the rate of the transmural wave front of progressing necrosis after 20 minutes of ischemia.
D000818:Animals; D003326:Coronary Circulation; D003327:Coronary Disease / Q000378:metabolism*; D004285:Dogs; D004699:Endocardium / Q000378:metabolism / Q000473:pathology; D005260:Female; D006321:Heart / Q000503:physiopathology; D006439:Hemodynamics; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D009336:Necrosis; D010496:Pericardium / Q000378:metabolism / Q000473:pathology