Aim: 

Apelin-13 (A-13) is an endogenuos ubiquitary peptide which acts as a ligand of a G-protein coupled APJ receptor. On the cardiovascular system it reduces peripheral resistence, increases myocardial inotropy and is reported to pretect the heart against the extention of ischemia/reperfusion (I/R) injury if given after ischemia, while no data are available if given before. We investigated whether the protection occurs in the latter case.

Methods: 

Isolated rat hearts perfused with oxygenated Krebs-Henseleit buffer underwent 30 min of global ischemia and 120 min of reperfusion. Ventricular pressure was measured from a baloon in the left ventricle. Infarct size was determined with nitro-blue-tetrazolium.Ten hearts did not receive A-13 and were used as controls. In two groups of 5 hearts A-13 with the buffer at a concentration of 500 nM for 20 min before and after ischemia respectively. Statistical significance was assessed with one-way ANOVA.

Results: 

Data are expressed as mean ±SE. Being 54±3% in the controls, infarct size decreased to 45±5% (p<0.05) if A-13 was infused before and 26±6% (p<0.001) if given after ischemia. Developed pressure recovered significantly (p<0.01) only with A-13 after ischemia.

Conclusion: 

We conclude that A-13 protects against I/R injury if given either before or after ischemia. However after ischemia it is more effective and improves mechanical recovery.The different effect is likely to be related to the increase in APJ receptors which is reported to occur after ischemia.