Comparison of renal extraction efficiencies for radioactive agents in the normal dog.

The renal extraction efficiencies for various radioactive agents were measured in normal anesthetized dogs during 1 hr after a single intravenous injection. Radioassays were made on serial blood samples drawn simultaneously from the aorta upstream from the renal arteries and from one renal vein. As a reference substance [131I]o-iodohippurate was injected concurrently in all experiments. Blood clearances from serial venous samples and urinary excretion also were measured. Extraction efficiency from whole blood was calculated as (A-V) divided by A, where A = aortic concentration and V = renal venous concentration. This ratio for commercial [131I]o-iodohippurate fell steadily from 88% at 30 sec to 50% at 1 hr. For "purified" [131I]o-iodohippurate the fall was less marked, to 61% at 1 hr. The EE ratios for all other agents were stable after the first minute. The Tc-99m complexes of DTPA, glucoheptonate, and acetylcysteine had ratios averaging 27-29%. The ratios of Tc-99m DMS and Hg-197 chlormerodrin had much lower average values of 8 and 14%, respectively. None of the newer agents approached the extraction efficiency of [131I]o-iodohippurate.

Distribution of leukocytes labeled with In-111 oxine in dogs with acute inflammatory lesions.

The biodistributions of In-111 oxine (with and without leukocyte labeling) of Ga-67 citrate and of In-111 chloride were compared in 30 dogs with chemical and bacterial abscesses and acute joint inflammation. Serial blood samples were taken and tissues radioassayed at 24 hr. The concentration of In-111-oxine leukocytes in all three types of inflammatory lesion was invariably much higher than that of Ga-67 injected simultaneously. For bacterial abscesses, the mean abscess-to-muscle concentration ratio was 3,000 for labeled leukocytes and 72 for Ga-67. Aqueous buffered In-111 oxine sulfate solution appeared better for labeling leukocytes than In-111 oxine in ethanol. When In-111 oxine was not incubated with leukocytes before injection, or if the cells were poorly labeled or damaged, the abscess localization was often inferior to that of gallium. Localization of In-111 chloride also appeared inferior to that of gallium. No significant difference in distribution in the major organs or inflammatory lesions was demonstrable between labeled suspensions of "pure"neutrophils harvested by elutriation and "mixed"cell suspensions of leukocytes after erythrocyte sedimentation with hydroxyethyl starch. For both types of leukocyte suspension labeled with In-111 oxine, the average recovery of cell-bound activity in the circulating blood at 4 hr was 32% of the administered activity, inferior to that of DFP-32. It is concluded, therefore, that In-111 oxine is a more effective agent than Ga-67 for the detection of acute focal inflammatory lesions if leukocytes are properly labeled, but current techniques are unsatisfactory for the study of neutrophil kinetics.

Labeling of platelets with oxine complexes of Tc-99m and In-111. Part 1. In vitro studies and survival in the rabbit.

We have used both Tc-99m oxine and In-111 oxine to study the effects in the rabbit of various parameters on platelet labeling and the in vivo survival of platelets harvested by four different methods. For In-111 oxine, platelet labeling in saline produces much higher efficiencies (90%) than labeling in the presence of plasma (20%), with no significant shortening of in vivo survival (1% survival at 5.9 days). For Tc-99m oxine, labeling efficiencies are considerably lower (30%) and survival is shorter (1% survival at 3.8 days). For both radioagents, a 30-min labeling incubation at room temperature is suggested.

Platelets labeled with oxine complexes of Tc-99m and In-111. Part 2. Localization of experimentally induced vascular lesions.

Using rabbit platelets harvested and labeled with either Tc-99m or In-111 oxine as described in Part 1, we have successfully imaged experimentally induced fresh venous thrombi and newly injured arterial intima. Visualization of lesions up to 6 hr old is striking. Thrombi and arterial damage 24 hr old, however, were usually not imaged successfully; nor were preformed platelet-poor arterial emboli. The varying rates of platelet deposition in vascular lesions of different ages and types account for these observations. Should human cells prove as effective, widespread clinical application is anticipated.