Prolonged arterial occlusion caused by thrombus development at sites of arterial bifurcation.

Although thrombogenic atheromas frequently develop at sites of arterial branching or bifurcation, the nature of such thrombus formation remains unclear. In this study, small rat mesenteric arteries (about 0.3 mm id) were observed using a video-microscope system. Exposure of the media by inducing compression damage over a short segment caused occlusive thrombus formation and subsequent spontaneous reperfusion repeatedly over about 30 min. Compression damage was induced either at a site just distal to the bifurcation (group 1, n = 7) or 5-10 mm downstream from the bifurcation (group 2, n = 7). The number of thrombotic occlusions was similar in the 2 groups, but the total duration of occlusion was significantly higher in group 1 (540 +/- 47 sec) than in group 2 (295 +/- 24 sec) (p < 0.01). The total duration of occlusion in group 1 was significantly reduced to 273 +/- 16 sec (p < 0.01) by mechanical interruption of flow in the other, intact, arterial branch. In the presence of blood flow through the intact branch, the occlusive thrombus at the bifurcation further enlarged in the direction of the intact branch, resulting in a significantly larger thrombus than in the absence of blood flow (17.1 +/- 2.1 vs 9.2 +/- 0.9 x 10(-2) mm2, p < 0.01). Stasis of the arterial blood per se did not affect the duration of thrombotic occlusion or increase plasma fibrinolytic activity. Thus, arterial occlusion caused by a thrombus arising at arterial bifurcations may be prolonged because of enlargement of the thrombus owing to the action of platelets in blood flowing through the intact branch.