Kazuo Nitta

Mechanism of gallium 67 accumulation in inflammatory tissue

The present study was undertaken to elucidate the accumulation mechanism of gallium 67 in inflammatory tissue.67Ga accumulation in inflammatory tissue was observed by macro- and microautoradiogram. Permeability indices were calculated for serum albumin from blood vessels into inflammatory and normal tissue. Neutrophils and macrophages did not play a major role in67Ga accumulation in the inflammatory tissue because67Ga could hardly be detected in the sites in which neutrophils were crowded; the accumulation was concentrated in the intercellular space around these cells in the tissue. Permeability indices for inflammatory tissue were much greater than those for normal tissues. It is thought from the present study and previously reported results that67Ga, together with plasma from permeable blood vessels, readily penetrates the inflammatory tissue and stays there by binding to the acid mucopolysaccharide present in the tissue.

67Ga-binding substances in abscess and normal tissues.

Abscess-induced animals and normal animals were treated with 67Ga-citrate. Abscess, kidney, heart, lung, and spleen were excised and homogenized. After removal of the nuclear fraction, each of these homogenates was digested with protease. After digestion, the supernatants of the reaction mixtures were applied to a Sephadex G-100 column. Resultant eluates were analyzed for radioactivity, protein, uronic acids, and sialic acids. Sodium sulfate-25S was administered to animals that were then treated by the same procedure as that followed for animals treated with 67Ga-citrate. In abscess, kidney, lung, heart, and spleen, sizeable amounts of 67Ga had been bound to the sulfated acid mucopolysaccharides with molecular weights of about 10,000, and to the sulfated acid mucopolysaccharides, a species whose molecular weights exceeded 40,000. Based on the results presented here, it is clear that 67Ga-binding substances in abscess and also in the above four organs are sulfated acid nucopolysaccharides.

67Ga accumulation in inflammatory lesion and its mechanism: Comparison with malignant tumor

The accumulation of 67Ga in inflammatory lesions increased with time after injection of turpentine iol and reached a plateau 5 days later. At that time the uptake in the lesions was larger than any other tissue, after ten days the lesion uptake decreased. In experiments using rats which had been kept for 5 days after subcutaneous injection of turpentine oil, the accumulation of 67Ga in inflammatory lesions increased with time until six days after administration of 67Ga-citrate. It is clear from this study that 67Ga is avidly accumulated in areas where the subcutanous tissue is infiltrated with neutrophils and macrophages, that it is not accumulated at the sites in which neutrophils are crowded, that nuclear material, mitochondria, lysosomes and microsomes do not play a major role in 67Ga accumulation in the lesion and that the main binding acid mucopolysaccharide in the lesion is acid mucopolysaccharide which is none of the following: keratan sulfate, heparan sulfate, heparin, or chondroitin sulfate A, B or C. It is presumed that the main 67Ga binding acid mucopolysaccharide is keratan polysulfate (or other oversulfated acid mucopolysaccharides).

Distribution of 67Ga-citrate in abscess-induced rat by quantitative whole body autoradiography

Distribution of 67Ga-citrate in inflammatory tissues was determined, and correlation between the 67Ga-uptake and capillary permeability of plasma from blood vessels in the inflammatory tissue was elucidated, by quantitative whole body autoradiography and double tracer autoradiography. The distribution of 67Ga in inflammatory tissue was similar to that of 131I-HSA and 99mTc-HSA, which were applied as an index to the plasma element. These results showed that the capillary permeability of plasma from blood vessels in the inflammatory tissue increases, and this causes the 67Ga-uptake.

Study of the Biological Function Using Several Radioactive Iodines and its Clinical Application

異なった核種の放射性ヨウ素で標識した蛋白を同時に投与することによって, 同一患者の同一時点における蛋白代謝を比較しようとした。すなわち, 125I-標識アルブミン, 131I-標識γ-グロブリンを正常, 肝硬変症, ネフローゼ症候群, malabsorption syndrome患者に同時に静注し, また, 2種の131I, 125I-標識パラプロテインを形質細胞腫患者に投与して, 125I, 131Iを分離測定することにより, その血漿放射能消失関係をもとめ, その数学的解析をおこなった。125Iおよび131Iは, 化学的分離操作をおこなうことなく, liquid scintillation spectrometerの波高分析回路とwell typeシンチレーション検出器とを組合わせた装置を用いて測定操作によって分離した。