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Updated: May 4, 2026
Glutamate and Hypoxia as a Stress Model for the Isolated Perfused Vertebrate Retina
Published on: March 22, 2015
Increasing glutamate promotes ischemia-reperfusion-induced ventricular arrhythmias in rats in vivo
Xianlin Sun1, Jingquan Zhong, Deguo Wang
1Department of Cardiology, Anhui Provincial Hospital of Anhui Medical University, Hefei, PR China.
Background:
Glutamate mediates cerebral ischemia injury via N-methyl-D-aspartate (NMDA) receptor-coupled ion channels, but the activities of glutamate in the heart remain unclear.
Aims:
To investigate whether or not glutamate contributes to ischemia- and reperfusion (IR)-induced arrhythmias.
Methods:
Myocardial IR was induced by occlusion of the left anterior descending coronary artery for 30 min and reperfusion for another 30 min. A score system was used to quantify arrhythmias. MK801 (a noncompetitive NMDA receptor antagonist), dihydrokainate (DHK, a glutamate transporter inhibitor) and gabapentin (GBP, a glutamate release inhibitor) were used before ischemia. Serum glutamate levels, Ca(2+)-ATPase activity, SERCA2a protein expression and myocardial mitochondrial Ca(2+) content were assayed.
Results:
Myocardial IR caused a significant increase in serum glutamate and high incidences of ventricular arrhythmias. GBP and MK801 significantly ameliorated ventricular arrhythmias, improved SERCA2a expression and sarcoplasmic reticulum Ca(2+)-ATPase activity and reduced Ca(2+) accumulated in mitochondria. By contrast, DHK significantly exacerbated reperfusion-related arrhythmias and mitochondrial Ca(2+) overload while it decreased SERCA2a expression and activity.
Conclusion:
This study showed that glutamate mediates reperfusion arrhythmias, and the corresponding mechanism may be associated with Ca(2+) overload via the NMDA receptor. Reperfusion arrhythmias may be prevented by inhibiting the release of glutamate or by antagonizing NMDA receptors.
