Heyns A D, Lötter M G, Badenhorst P N, van Reenen O, Pieters H, Minnaar P C
Thromb Haemost. 1980 Oct 31;44(2):100-4.
The survival, tissue distribution and fate of (111)Indium-oxine labelled autologous platelets was studied in four asplenic subjects with serial blood sampling, scintillation camera and computer-assisted imaging. Mean (111)In-platelet recovery in the circulation was 89 /+- 13% (/+- 1 SD). Platelet survival curves fitted a linear function best and was 238 /+0 41 h. The shape of the survival curves of normal and asplenic subjects differed: in the asplenic subjects the curve was linear whereas that of normal subjects was significantly more curvilinear if analyzed by least squares computer fitting to a gamma function. Early hepatic (111)In-activity was significant and transient and ascribed to the "collection injury". As labelled platelets disappeared from the circulation, (111)In-activity in the liver increased progressively and linearly to reach 42.5 /+- 14.1% of whole body activity at 240 h. Radioactivity also accumulated in the bone marrow, but could not be demonstrated in the vasculature of the lower limbs. These results would indicate that in asplenic subjects the majority sites of destruction of senescent platelets are the liver and bone marrow.
通过连续采血、闪烁相机和计算机辅助成像，对4名无脾受试者中（111）铟-氧肟酸标记的自体血小板的存活、组织分布和转归进行了研究。循环中（111）铟标记血小板的平均回收率为89±13%（±1标准差）。血小板存活曲线最适合线性函数，为238±41小时。正常受试者和无脾受试者的存活曲线形状不同：在无脾受试者中，曲线是线性的，而正常受试者的曲线如果通过最小二乘法计算机拟合伽马函数进行分析，则明显更弯曲。早期肝脏的（111）铟活性显著且短暂，归因于“采集损伤”。随着标记血小板从循环中消失，肝脏中的（111）铟活性逐渐线性增加，在240小时时达到全身活性的42.5±14.1%。放射性也在骨髓中蓄积，但在下肢血管中未得到证实。这些结果表明，在无脾受试者中，衰老血小板的主要破坏部位是肝脏和骨髓。
