Mitochondrial structure and function in acute myocardial ischemic injury.
Changes in both the structure and function of mitochondria occur in the dog heart as a consequence of severe ischemia produced by acute coronary occlusion. Brief periods of severe ischemia (reversible injury) produced no significant change in mitochondrial ultrastructure and no defects in pyruvate or succinate metabolism. However, periods of ischemia of 40-60 minutes' duration (irreversible injury) produced striking structural changes including swelling, an increase in matrix space, disorganization of cristae, and the appearance of amorphous matrix densities. After 60 minutes of severe ischemia, one or more amorphous densities were present in each mitochondrial profile. These osmiophilic structures contained lipid but have not been characterized further. Their presence was typical of the irreversible state. Mitochondria of irreversibly injured cells were fragile, and consequently were more difficult to isolate than mitochondria of control tissue. Furthermore, after isolation from tissue injured by 60 minutes of ischemia, they showed markedly defective function.
D000818:Animals; D003327:Coronary Disease / Q000473:pathology* / Q000503:physiopathology; D004195:Disease Models, Animal; D004285:Dogs; D066298:In Vitro Techniques; D008931:Mitochondria, Muscle / Q000378:metabolism / Q000648:ultrastructure*; D008933:Mitochondrial Swelling; D009206:Myocardium / Q000378:metabolism / Q000648:ultrastructure*; D010101:Oxygen Consumption; D011773:Pyruvates / Q000378:metabolism; D013385:Succinate Dehydrogenase / Q000378:metabolism; D013386:Succinates / Q000378:metabolism
D011773:Pyruvates; D013386:Succinates; D013385:Succinate Dehydrogenase