Myocardial and pulmonary uptake of S-1'-[18F]fluorocarazolol in intact rats reflects radioligand binding to β-adrenoceptors

Article abstract of DOI:10.1016/0014-2999(94)00636-L

The biodistribution of S-(-)-4-(2-hydroxy-3-(1'-[¹⁸F]fluoroisopropyl)- aminopropoxy)carbazole ([¹⁸F]S-fluorocarazolol, a non-selective β-adrenoceptor antagonist) was studied in rats (60 min after ¹⁸F injection when specific binding in peripheral organs was maximal). ¹⁸F uptake in brain, erythrocytes, heart and lung appeared to be linked to β-adrenoceptors. CGP-20712A and ICI-89,406 inhibited ¹⁸F uptake in heart (predominantly, β₁-adrenoceptors) more potently than in lungs (predominantly β₂-adrenoceptors). In contrast, ICI-118,551 and procaterol were more potent in the lungs than in the heart. ICI-118,551 inhibited F uptake in cerebellum (predominantly, β₂-adrenoceptors) more potently than in cerebral cortex (predominantly, β₁-adrenoceptors). Stereoselectivity of the in vivo binding was demonstrated since S-(-)-propranolol inhibited uptake in target tissues more effectively than R-(+)-propranolol. Myocardial and cerebral imaging may be hampered by poor heart-to-lung contrast and low signal-to-noise ratios, but [¹⁸F]S-fluorocarazolol seems suitable for positron emission tomography (PET) of pulmonary, β-adrenoceptors.