Specificity of localization of myosin-specific antibody fragments in experimental myocardial infarction. Histologic, histochemical, autoradiographic and scintigraphic studies.

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Abstract
Concentration of radioiodinated (Fab'')2 fragments of cardiac specific antimyosin antibody in myocardial infarcts was previously shown to be inversely proportional to regional myocardial blood flow. Myocardial localization of antibody fragments has also been visualized by gamma camera scintigraphy. The site of 125I-antimyosin (Fab'')2 uptake with histochemical and histologic evidence of myocardial infarction was correlated. One mCi of 125I-antimyosin (Fab'')2 was administered i.v. 4 h after left anterior descending coronary artery ligation to anesthetized dogs. The dogs were allowed to recover for 48 h. The hearts were then excised, perfused with 1% triphenyl tetrazolium chloride (TTC) and formalin-fixed. One cm-thick transverse slices were cut; .gamma.-scintigrams for 125I-antimyosin (Fab'')2 localization, macro- and microautoradiograms and histologic studies were performed. Samples of the remaining tissues were assayed for 125I activity by gamma scintillation counting. Comparison of areas of 125I-antimyosin (Fab'')2 uptake on scintigrams and macroautoradiograms with TTC infarct location and size showed close correlation. Maximal ratios of 125I-antimyosin (Fab'')2 between infarcted and normal tissue (48 .+-. 13) were in the subendocardium at the infarct center in areas of most severe cellular necrosis. Microautoradiographic studies showed maximal grain density at the region of maximal myocyte necrosis. 125I-antimyosin (Fab'')2 localization is highly specific for necrotic myocardial cells.