Key result
Subepicardial burn injury in bullfrogs mimics human AMI ST changes, linked to decreased Na+/K+-ATPase expression.
Why the study?
Does subepicardial burn injury reproduce reciprocal ST segment changes in a bullfrog heart model?
Does subepicardial burn injury reproduce reciprocal ST segment changes in a bullfrog heart model?
A burn-induced subepicardial injury model in bullfrog hearts successfully reproduced reciprocal ST segment changes and demonstrated that decreased Na+/K+-ATPase expression in injured cardiomyocytes may be responsible for the 'currents of injury'.
Subepicardial burn injury reproduces reciprocal ST changes in bullfrogs; leaves open translation to human AMI mechanisms or ECG interpretation.
In our previous studies, by simply inducing burn injuries on bullfrog hearts or partially exposing their surface to high-potassium (K+) solution, we could reproduce a ST segment elevation in the electrocardiogram (ECG), which is a characteristic finding in human ischemic heart disease. In the present study, using our burn-induced subepicardial injury model, we could additionally reproduce “reciprocal” ST segment changes for the first time in frog hearts, mimicking those observed in human acute myocardial infarction. Immunohistochemistry demonstrated markedly decreased Na+/K+-ATPase protein expression in the ventricular surface after the burn injury. The loss of this pump expression in injured cardiomyocytes was thought to be responsible for the creation of “currents of injury” and the subsequent ST segment changes observed in acute myocardial infarction.
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Kazama et al. (2019) studied acute myocardial infarction (model). burn injury was evaluated on ST segment changes and Na+/K+-ATPase protein expression. Burn-induced subepicardial injury in bullfrog hearts reproduced reciprocal ST segment changes mimicking human acute myocardial infarction, associated with decreased Na+/K+-ATPase protein expression.
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