Prenen G H, Go K G, Paans A M, Zuiderveen F, Vaalburg W, Kamman R L, Molenaar W M, Zijlstra S, Elsinga P H, Sebens J B
Department of Neurosurgery, University of Groningen, The Netherlands.
Acta Neurochir (Wien). 1989;99(3-4):166-72. doi: 10.1007/BF01402328.
In cat brain with a freezing injury, the uptake of 1-11C-acetoacetate (11C-ACAC), 2-18F-fluorodeoxy-D-glucose (18FDG), and L-1-11C-tyrosine (11C-TYR) was monitored by positron emission tomography following intravenous administration of the tracers, at 1 day, and 1-3 weeks after the injury. The development and further course of the cold-induced oedema was monitored by magnetic resonance imaging. In the fresh (1 day old) lesion there was increased uptake of 11C-ACAC, probably due to release of the restrictive influence of the blood-brain barrier upon passage of the substance into brain. The uptake of 18FDG, which normally occurs by carrier-mediated transport at the barrier, was decreased in the fresh lesion, probably as a result of damage of the carrier mechanism. In the 3 week old lesion 18FDG uptake was still reduced, and 11C-ACAC uptake was still increased, although barrier function to Evans blue had recovered. It is suggested, that the increased 11C-ACAC uptake in the chronic lesion bears upon the proliferation of macrophages and reactive glial cells in the lesion. This is supported by the increased uptake of 11C-TYR in the 2 weeks old lesion, while in the fresh lesion 11C-TYR uptake was unchanged.
在患有冷冻损伤的猫脑中，静脉注射示踪剂后，于损伤后1天以及1 - 3周，通过正电子发射断层扫描监测1-¹¹C-乙酰乙酸盐（¹¹C-ACAC）、2-¹⁸F-氟脱氧-D-葡萄糖（¹⁸FDG）和L-1-¹¹C-酪氨酸（¹¹C-TYR）的摄取情况。通过磁共振成像监测冷诱导水肿的发展及后续过程。在新鲜（1日龄）损伤灶中，¹¹C-ACAC摄取增加，这可能是由于血脑屏障对该物质进入脑的限制作用解除所致。通常通过载体介导在屏障处转运的¹⁸FDG摄取在新鲜损伤灶中减少，这可能是载体机制受损的结果。在3周龄损伤灶中，尽管对伊文思蓝的屏障功能已恢复，但¹⁸FDG摄取仍降低，¹¹C-ACAC摄取仍增加。有人提出，慢性损伤灶中¹¹C-ACAC摄取增加与损伤灶中巨噬细胞和反应性胶质细胞的增殖有关。这得到了2周龄损伤灶中¹¹C-TYR摄取增加的支持，而在新鲜损伤灶中¹¹C-TYR摄取未改变。
