Following coronary occlusion in a canine model, both infarcted and uninfarcted myocardium demonstrate increased protein synthesis, reflecting reparative mechanisms and compensatory energy utilization.
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Highlights post-infarct protein synthesis in canine myocardium; leaves open translation to human remodeling or therapy.
Myocardial protein metabolism was studied in dogs with coronary occlusion produced by ligating the anterior descending coronary artery. On the muscle homogenates obtained from the infarcted area and the uninfarcted one concentrations of nitrogenous substances and some enzymes related to protein metabolism were measured at various time intervals up to 7 days after coronary occlusion. Electrocardiographic and histological observations were also demonstrated. In the infarcted muscle, were observed considerable changes in the structural proteins which reflect the patho-anatomical changes. The infarcted tissue showed an increase in protein synthesis. This is one of the reparative mechanism after infarction. In the uninfarcted muscle, changes in the protein composition were observed, which suggest an increase in production and utilization of energy as well as the acceleration of protein synthesis.
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Akihisa Takahashi (1967) studied this question.
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