Kazama Itsuro, Sonobe Hiroyuki
School of Nursing, Miyagi University, Miyagi, Japan.
J Vet Med Sci. 2025 Jul 1;87(7):763-768. doi: 10.1292/jvms.25-0127. Epub 2025 May 15.
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 (HO). The ECG showed a marked elevation of the ST segments, and the action potential in cardiomyocytes demonstrated shortening of its duration. HO exposure did not affect the abundance of K channel proteins. However, pharmacological blockade by glibenclamide significantly suppressed HO-induced changes in ECG and tended to suppress cardiac action potentials. K channel stimulation by HO is thought to be responsible for generating an electrical difference in cardiomyocytes and the subsequent ST segment elevation.
缺血再灌注损伤是由血管再通后活性氧的产生引起的。其特征是心电图(ECG)上ST段抬高,尽管其机制尚不清楚。在本研究中,我们通过将牛蛙心脏暴露于过氧化氢(HO)来再现缺血再灌注损伤期间观察到的ST段变化。心电图显示ST段明显抬高,心肌细胞的动作电位持续时间缩短。HO暴露不影响钾通道蛋白的丰度。然而,格列本脲的药理学阻断显著抑制了HO诱导的心电图变化,并倾向于抑制心脏动作电位。HO对钾通道的刺激被认为是导致心肌细胞产生电差异以及随后ST段抬高的原因。