Tsan M F, Chen W Y, Scheffel U, Wagner H N
J Nucl Med. 1978 Jan;19(1):36-43.
The mechanism of ionic gallium-67 localization in inflammatory lesions was studied. Human polymorphonuclear leukocytes (PMN) had higher Ga-67 uptake than lymphocytes, whereas red blood cells had no affinity for Ga-67. Uptake by PMN showed temperature dependence, was independent of Ga-67 concentrations, and was not inhibited by metabolic inhibitors. However, its binding to PMN could be removed by trypsin but not by neuraminidase. These results are consistent with the hypothesis that the plasma membrane serves as a diffusion barrier and Ga-67 only binds to the surface of the PMN plasma membrane. When this membrane's permeability barrier was disrupted, as in heat-killed PMN, Ga-67 uptake increased markedly. Experimental abscesses were induced with E. coli or turpentine in rabbits. Twenty-four hours after i.v. injection, only 20% of Ga-67 in abscesses was in fractions containing intact PMN, cell debris or bacteria; the remainder was in a soluble, non-cellular fraction (2,500-g supernatant).
对离子态镓 - 67在炎症病灶中的定位机制进行了研究。人类多形核白细胞（PMN）对镓 - 67的摄取高于淋巴细胞，而红细胞对镓 - 67没有亲和力。PMN的摄取表现出温度依赖性，与镓 - 67浓度无关，且不受代谢抑制剂的抑制。然而，其与PMN的结合可被胰蛋白酶去除，但不能被神经氨酸酶去除。这些结果与以下假设一致，即质膜作为扩散屏障，镓 - 67仅与PMN质膜表面结合。当该膜的渗透屏障被破坏时，如热灭活的PMN，镓 - 67摄取显著增加。用大肠杆菌或松节油在兔子身上诱导实验性脓肿。静脉注射24小时后，脓肿中只有20%的镓 - 67存在于含有完整PMN、细胞碎片或细菌的组分中；其余部分存在于可溶性非细胞组分（2500g离心上清液）中。
