Hydrogen peroxide exposure to bullfrog heart causes ST segment elevation

Ischemia-reperfusion injury is caused by reactive oxygen production after revascularization. It is characterized by elevated ST segments on electrocardiogram (ECG), although the mechanisms remain unknown. In the present study, we reproduced the ST segment changes observed during ischemia-reperfusion injury by exposing bullfrog hearts to hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>). The ECG showed a marked elevation of the ST segments, and the action potential in cardiomyocytes demonstrated shortening of its duration. H<sub>2</sub>O<sub>2</sub> exposure did not affect the abundance of K<sub>ATP</sub> channel proteins. However, pharmacological blockade by glibenclamide significantly suppressed H<sub>2</sub>O<sub>2</sub>-induced changes in ECG and tended to suppress cardiac action potentials. K<sub>ATP</sub> channel stimulation by H<sub>2</sub>O<sub>2</sub> is thought to be responsible for generating an electrical difference in cardiomyocytes and the subsequent ST segment elevation.

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Publication Details

Journal
Journal of Veterinary Medical Science
Published
2025-01-01
DOI
https://doi.org/10.1292/jvms.25-0127
Citations
1
Primary Topic
Analytical Chemistry and Sensors
Type
article
Field-Weighted Citation Impact
0.74
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article

Hydrogen peroxide exposure to bullfrog heart causes ST segment elevation

Hiroyuki Sonobe, Itsuro Kazama
1 citations
Journal of Veterinary Medical Science
Analytical Chemistry and Sensors
0.74
article

Hydrogen peroxide exposure to bullfrog heart causes ST segment elevation

Hiroyuki Sonobe, Itsuro Kazama
article en
1 citations

Abstract

Ischemia-reperfusion injury is caused by reactive oxygen production after revascularization. It is characterized by elevated ST segments on electrocardiogram (ECG), although the mechanisms remain unknown. In the present study, we reproduced the ST segment changes observed during ischemia-reperfusion injury by exposing bullfrog hearts to hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>). The ECG showed a marked elevation of the ST segments, and the action potential in cardiomyocytes demonstrated shortening of its duration. H<sub>2</sub>O<sub>2</sub> exposure did not affect the abundance of K<sub>ATP</sub> channel proteins. However, pharmacological blockade by glibenclamide significantly suppressed H<sub>2</sub>O<sub>2</sub>-induced changes in ECG and tended to suppress cardiac action potentials. K<sub>ATP</sub> channel stimulation by H<sub>2</sub>O<sub>2</sub> is thought to be responsible for generating an electrical difference in cardiomyocytes and the subsequent ST segment elevation.

Journal of Veterinary Medical ScienceVol. 87(7)
Miyagi University (JP)
Zero hunger
Openalex Percentile: Top 33%
Analytical Chemistry and Sensors
0.74
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