In a lab experiment with isolated rat hearts, the synthetic peptide KP-102 (a growth‑hormone‑releasing peptide) helped the hearts recover better after a short period of no blood flow. It lowered the pressure that builds up inside the heart and improved the heart’s pumping strength, without changing heart rate. These benefits happened even though the peptide wasn’t making more growth hormone.

KP-102, a synthetic growth hormone (GH)-releasing peptide, exerts a variety of effects on cardiac function. In the present study, we investigated the direct cardiac effects of KP-102 with regard to ischemia/reperfusion injury by using isolated rat hearts. Isolated Wistar rat hearts were mounted on a Langendorff apparatus and subjected to 30 min of ischemia followed by 40 min of reperfusion. The rat hearts were treated with 0.1-10 nmol/l KP-102 beginning from 15 min before ischemia until the end of the experiment, with the exception of the ischemia period. Cardiac parameters such as the left ventricular end-diastolic pressure (LVEDP), left ventricular developed pressure (LVDP), maximum dP/dt (+dP/dtmax), minimum dP/dt (-dP/dtmax), and heart rate (HR) were measured. The following ischemia/reperfusion-induced cardiac dysfunctions were observed: increased LVEDP and decreased LVDP, +dP/dtmax, and -dP/dtmax. KP-102 at a dose of 0.1 nmol/l or more induced lower LVEDP and higher LVDP and gave higher +dP/dtmax and -dP/dtmax values during the reperfusion as compared with the control groups. In particular, KP-102 at 10 nmol/l clearly suppressed the increase in the LVEDP after reperfusion; eventually, the LVEDP was restored to the preischemia level. At 40 min of reperfusion, 10 nmol/l KP-102 noticeably increased the LVDP, +dP/dtmax, and -dP/dtmax, as compared with the control. KP-102 had no effect on the HR throughout the experiment. In conclusion, KP-102 improved cardiac function in rat isolated hearts subjected to ischemia/reperfusion injury, which is independent of GH secretion.