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  • Title: Quantitative thallium-201 redistribution with a fixed coronary stenosis in dogs.
    Author: Leppo J, Rosenkrantz J, Rosenthal R, Bontemps R, Yipintsoi T.
    Journal: Circulation; 1981 Mar; 63(3):632-9. PubMed ID: 7460249.
    Abstract:
    The redistribution of thallium-201 (201Tl) after coronary vasodilation was studied in 14 dogs with a proximal stenosis of the left circumflex coronary artery that did not reduce basal flow but attenuated reactive hypermia. During an 8-10-minute i.v. infusion of adenosine, radioactive microspheres and 201Tl were injected into the left atrium. Sequential cardiac scintiscans and microsphere injections permitted subsequent determination of coronary blood flow during the redistribution of 201Tl. After 15-220 minutes of observation, the dogs were killed and the hearts removed for the measurement of the activity of 201Tl and the radioactive microspheres in the normal (left anterior descending coronary artery [LAD]) and flow-restricted (left circumflex coronary artery [LCX]) regions. The ratios of the activity in LAD/LCX for microspheres (TRmic) and for 201Tl (RT1) were compared with the activity ratio determined from the scintiscan (Rscan). Rmic for the microsphere simultaneously injected with 201Tl can be compared with the initial Rscan, which showed a significant hourly decrease from an initial value of 1.26 +/- 0.12 to a mean final value of 1.02 +/- 0.09 by 3-4 hours. The final Rscan (mean 1.07 +/- 0.10) in each experiment also correlated significantly (r = 0.854) with the final true myocardial RT1 (mean 1.26 +/- 0.25). Rscan underestimated Rmic (average 2.25 +/- 0.48) when both 201Tl and microspheres were simultaneously injected; Rscan also underestimated RT1, but the directional changes were similar. A further analysis of the Rmic, Rscan and RT1 in two groups of dogs with either relatively high or low coronary flow during adenosine infusion suggests that the net loss of cellular 201Tl from the normal scintigraphic area is the mechanism underlying the resolution of these initial defects.
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