Janicek M J, Van den Abbeele A D, Hollenberg N K, Kassis A I, Holman B L, Tumeh S S
Department of Radiology, Harvard Medical School, Boston, Massachusetts.
Invest Radiol. 1990 Sep;25(9):988-93. doi: 10.1097/00004424-199009000-00005.
Although platelet activation and aggregation after endothelial injury are well documented, the time course of platelet deposition and the relationship between platelet aggregation and the release of vasoactive products have not been fully clarified in vivo. To study the effect of platelet vasoactive products, a collateral blood supply was induced by ligating the superficial femoral artery in male New Zealand white rabbits. Two weeks later, endothelial injury to the distal abdominal aorta was produced by cytologic brush or mimicked with a metal coil embolus. Platelet aggregation was assessed with indium-111 (111In)-labeled platelets, and scintigraphy demonstrated significant, progressive platelet deposition up to 3 hours after injury and evidence of residual activity 24 hours later. Angiography showed that the time course of peripheral vasoconstriction matched closely that of platelet deposition, indicating release of vasoactive substances from the aggregating platelets. These pathophysiologic changes secondary to endothelial injury may have significant implications for intravascular interventional procedures.
尽管内皮损伤后血小板的激活和聚集已有充分记载，但在体内血小板沉积的时间进程以及血小板聚集与血管活性产物释放之间的关系尚未完全阐明。为了研究血小板血管活性产物的作用，通过结扎雄性新西兰白兔的股浅动脉诱导侧支血液供应。两周后，用细胞刷造成腹主动脉远端的内皮损伤，或用金属线圈栓子模拟内皮损伤。用铟-111（111In）标记的血小板评估血小板聚集情况，闪烁扫描显示损伤后长达3小时血小板有显著的进行性沉积，24小时后仍有残留活性的证据。血管造影显示外周血管收缩的时间进程与血小板沉积的时间进程密切匹配，表明聚集的血小板释放了血管活性物质。这些继发于内皮损伤的病理生理变化可能对血管内介入操作有重大影响。
