Objective: To observe the correlation of the arterial remodeling at the reference site and the lesion site and the effect of granulocyte-macrophage colony-stimulating factor (GM-CSF) on arterial remodeling.
Methods: 28 healthy New Zealand White rabbits were randomized to 2 equal groups: GM-CSF group receiving subcutaneous injection of GM-CSF (10 microg x kg(-1)xd(-1)) for 7 days, and pure damage group given subcutaneous injection of equivalent normal saline foe 7 days. Seven days later the iliac arteries of all animals were damaged by balloon. 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 analyzed. Lumen area (LA), external elastic lamina area (EELA), and intimal plus medial areas (I + M) were measured at the lesion(L) and reference(R) sites.
Results: The NO levels 4 weeks later of the GM-CSF group was 98 +/- 10 micromol/L, significantly higher than that of the pure damage group (83 +/- 12 micromol/L, P < 0.05). Morphometric analysis showed that the LA(L) of the pure damage group was (0.87 +/- 0.40) mm2, significantly smaller than that of the GM-CSF group [(1.34 +/- 0.52) mm2, P < 0.05]. The I + M(L) of the pure damage group was (2.62 +/- 0.48) mm2, significantly greater than that of the GM-CSF group [(2.26 +/- 0.43) mm2, P < 0.05]. There was no statistical significance in the EEL(L) between the 2 groups [(3.48 +/- 0.80) mm2 versus (3.60 +/- 0.91) mm2, P > 0.05]. Morphometric analysis showed that the LA(R) of the pure damage group was (1.60 +/- 0.48) mm2, significantly smaller than that of the GM-CSF group [(1.99 +/- 0.54) mm2, P < 0.05], whereas there was no statistical significance in the I + M(R) between the 2 groups. In both groups, LA(R) was significantly correlated with LA(L) (r = 0.919, P < 0.001); and EELA(R) was significantly correlated with EELA(L) (r = 0.909, P < 0.001) and I + M(R) (r = 0.685; P < 0.001).
Conclusion: Remodeling affects both the lesion and the reference sites and appears to occur in parallel and proportionately at both sites. GM-CSF treatment increases re-endothelialization of the injured artery and inhibits unfavorable remodeling.
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