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

Mast cell infiltration of the arterial wall has been demonstrated in atherosclerotic vessels and implicated in coronary artery spasm. Spasm of vein bypass grafts has also been reported. In this study we performed vein bypass grafting of the carotid arteries in rabbits and examined the grafts for the presence of mast cells. We also determined vein graft vasoreactivity to histamine, 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 histamine 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 histamine (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 pyrilamine (10(-7) mol/L) and was not altered by the H2 receptor antagonist cimetidine (10(-5) mol/L). The decreased sensitivity of vein bypass grafts to histamine suggests receptor down-regulation and is possibly the result of increased histamine in the vein bypass grafts. The presence of mast cells and histamine receptors, as well as altered histamine sensitivity, in vein bypass grafts suggests that infiltration by these cells may contribute to vein bypass graft vasospasm.