The redistribution of thallium-201 (201TI) 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 20'TI were
injected into the left atrium. Sequential cardiac scintiscans and microsphere injections permitted subsequent
determination of coronary blood flow during the redistribution of 201TI. After 15-220 minutes of observation,
the dogs were killed and the hearts removed for the measurement of the activity of 201TI and the radioactive
microspheres in the normal (left anterior descending coronary artery [LAD]) and flow-restricted (left circumflex
coronary artery [LCXJ) regions. The ratios of the activity in LAD/LCX for microspheres (TRmic)
and for 201T1 (RT1) were compared with the activity ratio determined from the scintiscan (Rscan). Rmic for the
microsphere simultaneously injected with 201TI 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 R,can (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). R.,,n underestimated Rmic (average 2.25 ± 0.48) when both 201T1 and
microspheres were simultaneously injected; Rican also underestimated RT1, but the directional changes were
similar. A further analysis of the Rmic, Rican 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 201T1 from the normal scintigraphic
area is the mechanism underlying the resolution of these initial defects.