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Previous studies suggest that granulocyte colony‑stimulating factor (G‑CSF) can promote bone marrow derived progenitor cells to mediate cardiovascular repair, potentially reversing mechanical dysfunction in chronic ischaemic heart disease and post myocardial infarction. Two models were used in the present study both using a surgical ameroid constrictor to induce arterial stenosis. The first model used the carotid artery of rabbits. They were divided into high fat diet (inducing atherosclerosis) or normal fat diet (control) groups. Each was subdivided into surgical exposure group without constrictor, ameroid constrictor receiving normal saline or receiving G‑CSF 15 µg/kg/day. Endothelial markers of endothelial nitric oxide synthase and endothelin 1 were increased by the use of ameroid constrictor in both atherosclerotic and non‑atherosclerotic mice, however were not further altered by G‑CSF. Scanning electron microscopy indicated that ameroid constrictor application altered endothelial morphology from an oval shape to a round shape and this was more prominent in the atherosclerotic compared with the non‑atherosclerotic group. G‑CSF injection increased the number of endothelial cells in all groups. The second model used the left coronary artery of pigs. They were equally divided into following groups, receiving normal saline (control), G‑CSF 2.5 µg/kg/day (low dose), 5 µg/kg/day (medium dose) and 10 µg/kg/day (high dose) for 5 days. G‑CSF at a low or high dose worsened intimal hyperplasia however at a medium dose improved it. In conclusion, G‑CSF had no effect in a rabbit carotid artery model of atherosclerosis. Its effects on the porcine heart were dose‑dependent; arterial disease worsened at a low or high dose, but improved at a medium dose.

Effects of granulocyte colony‑stimulating factor on rabbit carotid and porcine heart models of chronic obliterative arterial disease