Exogenous GalR2 receptor agonist reduces reperfusion injury in isolated rat heart

Objective. To study the effect of exogenous GalR2 receptor agonist (peptide H-Trp-Thr-Leu-Asn-Ser-Ala-Gly-Tyr-Leu-Leu-Gly-Pro-βAla-His-OH) (G) on reperfusion injury after total ischemia in isolated rat heart model. Material and methods. Isolated hearts of Wistar rats perfused with Krebs-Henseleit solution (KHS) according to the Langendorff method were subjected to total normothermic ischemia and reperfusion. In the group G, rat heart was reperfused by KHS containing peptide 5 μg/ml within 10 min. No peptide was infused for further 20min reperfusion. Reperfusion by KHS was carried out in the control group. We estimated recovery of cardiac function and necrotic damage to cardiomyocytes. Results. Recovery of left ventricle pressure, heart rate, maximum rate of left ventricular contraction and relaxation (+dP/dt and — dP/dt, respectively) was more effective under the influence of G compared to the control group (p<0.05—0.01). End-diastolic pressure significantly decreased in the same group. Total release of creatine phosphokinase into perfusate was significantly less in the group G compared to the control group. Conclusion. These results indicate possible direct effect of G on myocardium. Lower cardiac reperfusion injury is associated with kinase cascades following activation of GalR2 receptor by G agonist.