Mast cell infiltration: a possible mechanism for vein graft XXXX .

@entity4444 @entity3361 @entity95 @entity8765 @entity2473 @entity112 @entity2553
Mast cell infiltration of the arterial wall has been demonstrated in atherosclerotic vessels and implicated in @entity3361 . @entity2473 of vein bypass grafts has also been reported. In this study we performed vein bypass grafting of the carotid arteries in @entity95 and examined the grafts for the presence of mast cells. We also determined vein graft vasoreactivity to @entity112 , to assess whether mediators of mast cells may have a functional role in vivo. In the control veins no mast cells were identified in 80 high-power fields (400X). In the vein bypass grafts an average of 2.6 +/- 0.8 (p = 0.01) mast cells were identified in the same number of high-power fields. Isometric tension studies of control vein and vein bypass grafts treated with @entity112 resulted in sigmoid dose-response curves. The ED50 for control vein was 4.69 +/- 0.63 X 10(-5) mol/L. Compared with control vein, the vein bypass grafts showed a rightward shift in the dose-response curve to @entity112 (ED50 11.6 +/- 1.7 X 10(-5) mol/L, p = 0.01). The histaminergic response in both vessels was blocked by the H1 receptor antagonist @entity8765 (10(-7) mol/L) and was not altered by the H2 receptor antagonist @entity4444 (10(-5) mol/L). The decreased sensitivity of vein bypass grafts to @entity112 suggests receptor down-regulation and is possibly the result of increased @entity112 in the vein bypass grafts. The presence of mast cells and @entity112 receptors, as well as altered @entity112 sensitivity, in vein bypass grafts suggests that infiltration by these cells may contribute to vein bypass graft @entity2553 .
