Klonizakis I, Peters A M, Fitzpatrick M L, Kensett M J, Lewis S M, Lavender J P
Br J Haematol. 1980 Dec;46(4):595-602. doi: 10.1111/j.1365-2141.1980.tb06017.x.
Platelets labelled with 111In displayed similar survival curves after incubation with 111In-oxine in plasma, plasma-saline and dextrose saline media. The use of autologous red cells to cushion platelets during high-speed centrifugation facilitated platelet resuspension without greatly affecting the duration of the labelling procedure. Quantitative scanning after reinjection of labelled platelets in haematologically normal subjects showed that, initially, splenic indium amounted to about 35% of the injected dose and hepatic indium about 12%; these levels rose only slightly over the subsequent duration of the platelet life span. Subtraction of the signal from indium in platelets thought to be normally pooled within the spleen from the total indium signal gave splenic indium uptake curves which reflected splenic platelet destruction. Initially, the sum of indium levels in spleen, liver and blood equalled 100% of the dose. Thereafter, the sum fell progressively at a rate thought to be approximately equal to the rate of bone marrow uptake.
用铟-111标记的血小板在血浆、血浆-生理盐水和葡萄糖盐溶液培养基中与铟-8羟基喹啉孵育后显示出相似的存活曲线。在高速离心过程中使用自体红细胞来缓冲血小板有助于血小板重悬,且不会对标记过程的持续时间产生太大影响。在血液学正常的受试者中重新注射标记血小板后的定量扫描显示,最初,脾脏中的铟约占注射剂量的35%,肝脏中的铟约占12%;在随后的血小板寿命期间,这些水平仅略有上升。从总铟信号中减去被认为正常聚集在脾脏内的血小板中的铟信号,得到反映脾脏血小板破坏的脾脏铟摄取曲线。最初,脾脏、肝脏和血液中的铟水平总和等于剂量的100%。此后,该总和以被认为大致等于骨髓摄取速率的速度逐渐下降。