Aim To investigate the effects of mast cells degranulation on plaque development and their possible mechanisms in animal experiments by dealing apolipoprotein E gene-knock out(apoE~(-/-)) mice which had been placed perivascular common carotid collars with mast cells degranulator-Compound 48/80. Methods 12-week-old male apoE~(-/-) mice were fed a western-type diet and operated with perivascular right common carotid collar placement.4 weeks after surgery,mice were divided into 2 groups with 20 mice each.The experimental mice were intraperitoneally injected with Compound 48/80,0.5 μg/g,every other day;the control mice received the same injection of an equal volume of D-Hank's.Thirty minutes after 4th injection,animals were sacrificed to obtain carotid sections.Sections were routinely stained with hematoxylin and eosin.Corresponding sections on separate slides were stained with toluidine blue and immunohistochemically with antibodies against a macrophage-specific antigen or α-smooth muscle actin. Results Administration of Compound 48/80 did not affect the lipid contents of mice serum.However,the percentage of degranulated mast cells(80.6% ±17.8% vs 13.5%±4.1%,p<0.01) and the activity of tryptase in serum(0.57±0.13 u/L vs 0.36±0.10 u/L,p<0.05) were significantly increased.There were no pathological changes in common carotids non-collar placement but atheromatous plaques occured in common carotids collar placement of both groups.Significant increase in plaque area of maximum cross section(58 500±7 500 μm~2 vs 8 600±2 800 μm~2,p<0.01),the degree of lumen stenosis(81%±15% vs 41%±12%,p<0.05) and the expressions of αsmooth muscle actin(1 219±364 iu vs 522±137 iu,p<0.05)and macrophage-specific antigen(426±133 iu vs 169±38 iu,p<0.05)were detected in plaque of common carotids collar placement in the experimental group. Conclusions Perivascular common carotid collar placement can accelerate atherosclerotic plaque formation in apolipoprotein E-knock out mice. Compound 48/80 increases plaque area of maximum cross section and the degree of lumen stenosis by promoting proliferation of smooth muscle cells and accumulation of macrophages.