Immunohistochemical change of actin in experimental myocardial ischemia. Its usefulness to detect very early myocardial damages.
Pathomorphological diagnosis of acute myocardial infarction has many problems in human autopsy materials less than 4 to 6 hours after clinical onset and in rats 2 to 3 hours after experimental coronary occlusion. Since immunohistochemical reaction depends on the antigen determinant site of the material, changes in the reaction may reflect alterations at the molecular level in myocardial fibers. With this consideration in mind, the effectiveness of diagnosing infarction at the earliest (possible) stage, and the changes of actin filaments were investigated through experiments, using immunohistochemical methods involving anti-actin antibodies produced from chicken gizzards in our laboratory. The left coronary arteries of rats were ligated to produce ischemia. Dehydrogenases were shown to be still present by triphenyltetrazolium chloride (TTC) reaction, but the anti-actin antibody reaction had disappeared in areas corresponding to the ischemic sites. However, on electron microscopic examination of these sites, actin fibers were clearly revealed. In the case of ischemia lasting for more than 6 hours, the anti-actin antibody reaction had disappeared, corresponding to the disappearance of the TTC reaction. At this stage, myocardial actin fibers were revealed by electron microscopic examination. These results indicate that ischemia induces some type of biochemical degeneration at the molecular level of myocardial actin, most likely the change of actin polymerization. Moreover, they show that the anti-actin antibody technique is capable of detecting such very early degenerative and ischemic changes proving itself to be better suited for determining the range and degree of early infarction.
Nishida
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Second Department of Pathology, Kinki University School of Medicine, Osaka, Japan.
Hiruma
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Hashimoto
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D000199:Actins / Q000032:analysis* / Q000378:metabolism; D000818:Animals; D015415:Biomarkers; D003327:Coronary Disease / Q000378:metabolism / Q000473:pathology*; D007124:Immunoenzyme Techniques; D007150:Immunohistochemistry / Q000379:methods; D008297:Male; D009203:Myocardial Infarction / Q000378:metabolism / Q000473:pathology*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D051381:Rats; D011919:Rats, Inbred Strains
D000199:Actins; D015415:Biomarkers