Cremer J E, Hume S P, Cullen B M, Myers R, Manjil L G, Turton D R, Luthra S K, Bateman D M, Pike V W
MRC Cyclotron Unit, Hammersmith Hospital, London, England.
Int J Rad Appl Instrum B. 1992 Feb;19(2):159-66. doi: 10.1016/0883-2897(92)90003-h.
PK 11195 is a selective ligand for the peripheral-type benzodiazepine binding site (PTBBS). There are few such sites in normal brain but their number increases in association with tissue necrosis. The time-course of appearance of PTBBS around a focally induced ischaemic lesion in frontal cortex of rat brain was established by autoradiography using [N-methyl-3H]PK 11195. Using this information and the same experimental model of ischaemia, the distribution of radioactivity after injection of carbon-11 (t1/2 = 20.3 min, beta+ = 99.8%) labelled PK 11195 was studied. The purpose was to synthesize [N-methyl-11C]PK 11195 and to test its suitability as a tracer for depicting the presence of PTBBS in ischaemic lesions. The time-profiles of distribution of radioactivity in brain regions after intravenous injection of tracer and the ratio of radioactivity in lesioned compared with unlesioned cortex were determined. Data for the temporal (days after lesion induction) and for the regional retention of radioactivity were consistent with independent evidence (autoradiographic and immunohistochemical) for the occurrence of increased numbers of PTBBS, predominantly in association with macrophages, in areas undergoing necrosis.
PK 11195是外周型苯二氮䓬结合位点（PTBBS）的选择性配体。正常大脑中此类位点较少，但在组织坏死时其数量会增加。利用[甲基-³H]PK 11195通过放射自显影确定了大鼠脑额叶局灶性缺血性损伤周围PTBBS出现的时间进程。利用这些信息以及相同的缺血实验模型，研究了注射碳-11（半衰期=20.3分钟，β⁺=99.8%）标记的PK 11195后放射性的分布。目的是合成[甲基-¹¹C]PK 11195并测试其作为描绘缺血性损伤中PTBBS存在的示踪剂的适用性。测定了静脉注射示踪剂后脑区放射性分布的时间曲线以及损伤皮质与未损伤皮质放射性的比值。损伤后不同时间（损伤诱导后天数）以及放射性区域滞留的数据与独立证据（放射自显影和免疫组织化学）一致，表明在发生坏死的区域PTBBS数量增加，主要与巨噬细胞有关。
