Glutamate release predicts ongoing myocardial ischemia of rat hearts

Glutamate metabolism is associated with myocardial ischemia-reperfusion, but it is not clear whether glutamate reveals ongoing ischemia (OI). We evaluated whether microdialysis would detect OI induced by coronary artery ligation in a rat cardiac transplantation model.

A total of 24 Fischer 344 rats underwent syngeneic heterotopic cardiac transplantation. Of these, 16 rats underwent ligation of the left anterior coronary artery (LAD) of the heart to induce ongoing ischemia (OI), of which eight grafts received intra-aortally Gabapentin (12 mg/graft), a glutamate-release inhibitor and eight grafts with transplantation only served as the control. With a microdialysis catheter samples for glucose, lactate, pyruvate, glutamate, and glycerol were analysed spectrophotometrically. Histology and aquaporin 7 evaluations were performed after graft harvesting.

Glutamate was elevated after 15 min of reperfusion in OI as compared with Control (14.31 +/- 5.03 microM vs 6.75 +/- 2.21 microM, p = 0.05), respectively. Glycerol remained high in OI (61.89 +/- 46.13 microM to 15.84 +/- 0.85 microM, p = ns) and low in Control (12.33 +/- 3.36 microM to 5.52 +/- 0.25 microM, p = ns). Gabapentin decreased glutamate release from 7.32 +/- 1.57 microM to 2.71 +/- 0.64 microM, (p < 0.05) and resulted in decrease of glycerol levels from 24.64 +/- 4.03 microM to 10.43 +/- 2.49 microM, (p < 0.05) in OI. The expression of aquaporin 7 and histology confirmed OI.

We suggest that glutamate release may be used as an early indicator of OI after cardiac arrest.