Radionuclide clearance techniques.
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This study quantified the binding of ionic calcium by contrast media with disodium edetate and trisodium citrate versus those with only calcium disodium edetate. First, calcium binding by sodium diatrizoate with calcium disodium edetate was measured using an ion-selective electrode at ionic strengths of .08, .16, and .80 molal. Significant binding of calcium was observed, and the probable reaction product is calcium chloride diatrizoate. Second, solutions were mixed containing Renografin 76 (or Hypaque 76) and NaCl at a physiologic ionic strength. The Renografin, which contains disodium edetate and trisodium citrate, caused significantly more binding than did the Hypaque. However, 60% of the drop in ionic calcium was observed with Hypaque and is related to the diatrizoate anion. The nonionic agent iopamidol produced no decrease in ionic calcium. Significant reductions in ionic calcium are produced by both the diatrizoate anion and by edetate and citrate additives.
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In order to determine the best method for routine measurement of glomerular filtration rate (GFR) in severe renal failure, we compared simultaneously the urinary clearances of [99mTc] diethylenetriaminepentaacetic acid (DTPA) (UD), [125I]iothalamate (UI), 24-hr creatinine clearance (UC) and plasma clearance of [99mTc]DTPA (PD), based on three plasma samples. In 60 studies in 22 patients with serum creatinine values of 2 to 8 mg/dl, UD and UI were almost identical: UD = 0.358 +/- 0.976 UI +/- 0.87 ml/min, r = 0.990. However, PD overestimated UD by a large and variable extent: PD = 11.3 +/- 0.843 UD +/- 5.5 ml/min, r = 0.694, and was inconsistent in sequential measurements in individual patients. UC also overestimated urinary isotope clearance: UC = 4.2 + 0.95 UI +/- 3.9 ml/min, r = 0.865. Sequential measurements of GFR in five patients with severe but stable renal failure (mean GFR 5.9 ml/min) showed an average standard deviation of only 0.83 ml/min. Thus both UD and UI appear to be reliable and precise measures of GFR in severe renal failure.
Administration of four different contrast media exerted slight but significant and prolonged effects on the hormonal thyroid status, in 53 euthyroid subjects (four subgroups), without any clinical expression of dysthyroidism. Changes in serum T3, rT3 and T4 demonstrated different trends for each iodinated compound, probably depending on the regulatory thyroid mechanisms, and CM pharmacokinetics. Plasma profiles of free fractions (FT3, FT4) slightly reflected consensual changes with circulating iodothyronines, at various time periods of study, demonstrating high correlation indexes with total fractions. The five hormones profiles correlation study suggest that different mechanisms could be responsible for some features encountered of "low T3 syndrome". These effects may be not only equivalent to giving various sources of iodide, but suggest more complex mechanisms. It is apparent that man has a remarkable and possibly unique system of homeostatic thyroid hormone regulation.
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Pulmonary inactivation of prostaglandin E2 (PGE2) was investigated in isolated perfused rat lungs during infusion of ionic and nonionic radiographic contrast media (RCM). When 100 nmol of [14C]-PGE2 was infused slowly into the pulmonary circulation, the ionic ioglycamate decreased the metabolism of PGE2, but other ionic (diatrizoate and ioxaglate) and nonionic RCM (iopamidol and metrizamide) had no significant effect. When a smaller amount of [14C]-PGE2 (10 nmol) was injected as a bolus the metabolism of PGE2 was decreased also by diatrizoate and ioxaglate, but not by iopamidol. After a similar bolus injection of 10 nmol of [14C]-PGE2, the efflux of radioactivity from the lungs was increased by diatrizoate, ioglycamate and ioxaglate but remained unchanged by iopamidol and metrizamide. The RCM infusion did not change the perfusion pressure. The present study indicates that ionic RCM decrease the inactivation of PGE2 in rat lungs and thus possibly increase the circulating level of this prostaglandin.
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