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Purpose  Clinical positron emission tomography (PET) imaging of the presynaptic norepinephrine transporter (NET) function provides valuable diagnostic information on sympathetic outflow and neuronal status. As data on the NET-targeting PET tracers [ 11 C]meta-hydroxyephedrine ([ 11 C]mHED) and [ 18 F]LMI1195 ([ 18 F]flubrobenguane) in murine experimental models are scarce or lacking, we performed a detailed characterization of their myocardial uptake pattern and investigated [ 11 C]mHED uptake by kinetic modelling.    Methods  [ 11 C]mHED and [ 18 F]LMI1195 accumulation in the heart was studied by PET/CT in FVB/N mice. To test for specific uptake by NET, desipramine, a selective NET inhibitor, was administered by intraperitoneal injection. [ 11 C]mHED kinetic modelling with input function from an arteriovenous shunt was performed in three mice.    Results  Both tracers accumulated in the mouse myocardium; however, only [ 11 C]mHED uptake was significantly reduced by excess amount of desipramine. Myocardial [ 11 C]mHED uptake was half-saturated at 88.3 nmol/kg of combined mHED and metaraminol residual. After [ 11 C]mHED injection, a radiometabolite was detected in plasma and urine, but not in the myocardium. [ 11 C]mHED kinetics followed serial two-tissue compartment models with desipramine-sensitive  K  1 .    Conclusion  PET with [ 11 C]mHED but not [ 18 F]LMI1195 provides information on NET function in the mouse heart. [ 11 C]mHED PET is dose-independent in the mouse myocardium at < 10 nmol/kg of combined mHED and metaraminol. [ 11 C]mHED kinetics followed serial two-tissue compartment models with  K  1  representing NET transport. Myocardial [ 11 C]mHED uptake obtained from PET images may be used to assess cardiac sympathetic integrity in mouse models of cardiovascular disease.

ejnmmi research

[11C]mHED PET follows a two-tissue compartment model in mouse myocardium with norepinephrine transporter (NET)-dependent uptake, while [18F]LMI1195 uptake is NET-independent