Background
This study aims to elucidate whether ghrelin mitigates acute heart injury induced by lower limb ischemia-reperfusion (I/R 30/120 min.) and Their protective effects cover cytokines and heart tissue damage.

Material and Methods
Forty rats were randomized into four groups: control (group 1), ischemia reperfusion(group 2), Ghrelin (group 3), shamm (group 4). Ghrelin was administered before ischemia. Samples were obtained for tumor necrosis factor-alpha(TNF-a), interleukin 6(IL-6) . Finding of heart injury were examined.Cardiac function was monitored, and histomorphologic features, degree ofmyocardial injury, level of ERS markers, and number of apoptotic cardiomyocytes were determined.

Results:
Compared with control group, THA I/R group showed significantly decreased cardiac function, seriously damaged myocardial tissue, increased number of apoptotic cells, and overexpression of mRNA and protein of ERS markers.preadministration of ghrelin in vivo (10_8 mol/kg, intraperitoneal injection greatly ameliorated the damaged heart function, attenuated myocardial injury and apoptosis, and decreased the expression of ERS markers: it decreased the mRNA and protein levels of glucose-regulated protein78 (GRP78) and C/EBP homologous protein (CHOP), with reduced caspase-12 protein expression.

Conclusion
In this acute heart injury model induced by I/R of the lower limbs, pretreatment with ghrelin significantly attenuated proinflammatory activities and parenchymal heart damage.Ghrelin directly inhibited the myocardial ERS response induced by tunicamycin or dithiothreitol in rat cardiac tissue. Ghrelin could protect the heart against I/R injury, at least in part, through inhibiting myocardial ERS.