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Technetium-99m-HMPAO, Technetium-99m-ECD and Iodine-123-IMP Cerebral Blood Flow Measurements with Pharmacological Interventions in Primates

AEC Institute for Life Sciences, University of Pretoria, Pretoria, South Africa Department of Pharmacology, Potchesfstroom University, Potchefstroom, South Africa Institute for Medicine, Research Centre, Jülich, Germany

Correspondence: For correspondence or reprints contact: Irene C. Dormehl, DSc, AEC Institute for Life Sciences, University of Pretoria, P.O. Box 2034, Pretoria 0001, South Africa.

ABSTRACT

Technetium-99m-bicisate ethyl cysteinate dimer (ECD) presents a different pattern from cerebral blood flow (CBF) in the subacute phase of cerebral infarction, as measured by PET, perhaps due to lack of oxygen and enzyme activity; this pattern is contrary to that of hexamethyl-propyleneamine oxime (HMPAO) but similar to that of N-isopropyl-[¹²³I]ß-iodoamphetamine ([¹²³I]IMP). This study explores possible CBF differences among HMPAO, ECD and IMP, with various relevant drug interventions. Methods: Anesthetized adult baboons were used in these SPECT studies. Four studies (n = 6 baboons for each study), one control study and three intervention studies involving intravenous acetazolamide, nimodipine infusion and intramuscular sumatriptan, were followed with ^99mTc-HMPAO, ^99mTc-ECD and [¹²³I]IMP. The split-dose method was used as follows. For each tracer, intervention data from the second SPECT (SPECT-2) after the second tracer injection (444 MBq) reflected a change in CBF with respect to the baseline SPECT (SPECT-1) data from the initial injection (222 MBq). These changes as a ratio, R (R = SPECT-2/SPECT-1 ), for each study, and the R values for each tracer were compared to R values from the corresponding control studies, yielding a quantitative estimate of drug effects. Results: There were no significant differences (p > 0.05) between HMPAO and ECD for the control, acetazolamide and sumatriptan studies, but there was indeed a difference between the two for the nimodipine study, indicating a nimodipine-dependent underestimation of CBF with ECD (and also with IMP), with respect to HMPAO. A further significant difference was that larger CBF increases were observed with acetazolamide, as measured with [¹²³I]IMP. Conclusion: This is a crucial observation for the clinical interpretation of CBF SPECT data and should direct the choice of tracer for a specific examination.

Key Words: drug-tracer interaction • CBF SPECT • baboon model