Electron microscopical and enzyme histochemical changes in the rat myocardium during prolonged autolysis.
The effect on rat myocardium of autolysis at 19 degrees C, for up to 20 days, was studied by electron microscopy and enzyme histochemistry. The enzymes studied included monoamine oxidase (MAO), sytochrome oxidase (CytO), non-specific esterase ((Ns.E.), phosphorylase (P-ase), succinate dehydrogenase (SDH) and various NAD- and NADP-linked dehydrogenases. The myocardium lost its histochemical P-ase activity within a few hours of autolysis, whereas the activity of all other enzymes remained quite normal for at least about 4 days, except that of MAO and SDH, which were normal for about 8 and 12 days, respectively. The myocardial cells lost activity of various enzymes in a patchy manner during prolonged autolysis and practically all histochemical enzyme activity disappeared within 20 days. The early period of autolysis was accompanied by rapid ultrastructural changes of myocardial cells. During prolonged autolysis the gross architecture of the myocardium was lost gradually by the 12th to 20th days. Mitochondria were the organelles most resistant to the effects of autolysis, and numerous mitochondria with morphologically solid inner and outer membranes were seen among the totally disintegrated myocardium 20 days after death. The loss of P-ase activity coincided with the loss of glycogen. The loss of MAO, SDH and CytO activities was not closely related to the morphological preservation of mitochondria, but, in accordance with other enzymes, was more closely related to the disintegration of the over-all myocardial structure. The present results showed that the architecture of the myocardium, and especially that of the mitochondria, was surprisingly resistant to the effects of autolysis at room temperature. Also several enzymes of the myocardium other than those examined so far maintained quite stable histochemically demonstrable activity during prolonged autolysis. These observations give support to the possibility of making the diagnosis of myocardial infarction at postmortem more accurate than with the present morphological and histochemical routine methods.
D000429:Alcohol Oxidoreductases / Q000032:analysis; D000818:Animals; D001329:Autolysis; D001344:Autopsy; D003576:Electron Transport Complex IV / Q000032:analysis; D004950:Esterases / Q000032:analysis; D005260:Female; D008931:Mitochondria, Muscle / Q000648:ultrastructure; D008995:Monoamine Oxidase / Q000032:analysis; D009203:Myocardial Infarction / Q000175:diagnosis; D009206:Myocardium / Q000201:enzymology / Q000648:ultrastructure*; D006005:Phosphorylases / Q000032:analysis; D051381:Rats; D013385:Succinate Dehydrogenase / Q000032:analysis; D013997:Time Factors
D000429:Alcohol Oxidoreductases; D013385:Succinate Dehydrogenase; D008995:Monoamine Oxidase; D003576:Electron Transport Complex IV; D006005:Phosphorylases; D004950:Esterases