Subepicardial burn injuries in bullfrog heart induce electrocardiogram changes mimicking inferior wall myocardial infarction

Figures

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  Fig. 1.. Detection of electrocardiogram (ECG) signals from the limb leads and induction of inferior wall burn injury in bullfrog heart. Needle electrodes, inserted into the upper and lower limbs of the frog, were connected to the ECG amplifier and the electrical signals were detected by a data logger. In one of the bipolar limb leads, such as in lead I, the left arm (L) electrode served as an exploring electrode (the positive pole) and the right arm (R) electrode as a reference electrode (the negative pole). Likewise, lead II detected the potential difference between the right arm and left leg (LF), while lead III detected the difference between the left arm and left leg. The right leg (RF) electrode served as an electronic reference to improve unwanted noise rejection. In augmented unipolar limb leads, such as in aVR, aVL and aVF, the electrode in the left arm, right arm and left leg respectively served as the positive pole, while the negative pole was composed by averaging the measurements from the other limb electrodes. To induce subepicardial burn injuries on the inferior wall of the myocardium, a heated glass capillary tube was repeatedly placed on the inferior part of the frog heart…

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  Fig. 2.. Changes in electrocardiogram (ECG) before and after burn injuries were induced on the inferior wall. ECG detected from the bipolar limb leads (I, II and III) and unipolar limb leads (aVR, aVL and aVF) before (left) and after burn injuries were induced on the inferior part of the ventricle (right).

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  Fig. 3.. Na+/K+-ATPase expression and the transmembrane action potential after burn injuries were induced in bullfrog heart. (A) Top: Masson’s trichrome staining in intact ventricular cardiomyocytes (Control) and those after the burn injury (Burned). Magnification × 20. bottom: Immunohistochemistry using an antibody for Na+/K+-ATPase α-1 subunit (brown), counterstained with hematoxylin in intact ventricular cardiomyocytes (Control) and those after the burn injury (Burned). Magnification × 20. (B) a: Suction electrode method was employed to monitor the transmembrane action potential. A negative pressure was applied to the recording electrode, which was placed on the surface of the frog heart ventricle and connected to the data logger. To induce subepicardial burn injury, the heated glass capillary tube was pressed onto the ventricular surface where the transmembrane action potential was recorded. b: The action potential of cardiomyocytes was recorded before (left) and after burn injuries were induced (right).

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  Fig. 4.. Mechanisms of reciprocal ST segment changes in inferior wall burn injury model. Leads II, III and aVF are expressed as if they observe (view) the heart from the inferior wall of the ventricle. When myocardial injury was induced on the inferior wall of the ventricular surface, the currents of injury flowed away from the views of the leads II, III and aVF (white arrows). Thus, electrocardiogram (ECG) vector during diastole was negatively deflected from the isoelectric line (arrows), making the ST segment appear elevated during systole (gray waveform). On the other hand, leads aVL and I are expressed as if they observe (view) the heart from the superior part of the ventricle, which is almost opposite to the direction of the lead III. When myocardial injury was induced on the inferior wall of the ventricle, the currents of injury flowed nearly towards the views of the leads aVL and I (white arrows). This caused the ECG vector to be positively deflected during diastole (arrows), making the ST segment appear depressed during systole (gray waveform).