Objective Arterial remodelling may also occur at the reference site. Resent studies showed that granulocyte-macrophage colony-stimulating factor (GM-CSF) could facilitate the repair of endothelium and reduce vascular inflammation. To observe the effect of granulocyte-macrophage colony-stimulating factor on arterial remodelling, we evaluated the remodelling at the reference site and the lesion site in rabbit model.
Methods 28 healthy New Zealand White rabbits were randomised to two groups (GM-CSF group and control group). GM-CSF group received a subcutaneous injection of GM-CSF (10 ug/kg/d), the control group were given a subcutaneous injection of equivalent saline. The iliac arteries of all animals were damaged by balloon after 7d. The levels of nitrogen monoxide (NO) were detected before and 4 weeks after angioplasty. Histological sections of iliac from rabbits killed 4 weeks after angioplasty were analysed. Luminal area (LA), external elastic lamina area (EEL), and intimal plus medial areas (I+M) were measured at the lesion (L) and reference (R) sites.
Results The NO level of the GM-CSF group was significantly higher than that of the control group after 4 weeks (97.69±10.21 vs 83.18±12.57 μmol/l). Morphometric analysis showed that the LA (L) of control group was smaller than that of the GM-CSF group (0.87±0.40 vs 1.34±0.52 mm2, p<0.05) and I+M (L) was greater than that of the GM-CSF group (2.62±0.48 vs 2.26±0.43 mm2, p<0.05). There was no difference in EEL (L) between the two groups (3.48±0.80 vs 3.60±0.91, p>0.05). Morphometric analysis also showed a smaller LA (R) in the control group (1.60±0.48 vs 1.99±0.54 mm2, p<0.05), whereas there was no difference in I+M (R) between the two groups. EEL (R) significantly correlated with LA (R), EEL (L), and I+M (R) in both groups combined (r=0.91, p<0.0001; r=0.909, p<0.0001; and r=0.685; p<0.0001, respectively). LA (R) also correlated with LA (L) (r=0.919; p<0.0001).
Conclusion Remodelling can affect both the lesion and the reference sites and appears to occur in parallel and proportionately at both sites. GM-CSF treatment increased reendothelialization of the injured artery and inhibited unfavourable remodelling.