MYOCARDIAL AND PULMONARY UPTAKE OF S-1'-[F-18]FLUOROCARAZOLOL IN INTACT RATS REFLECTS RADIOLIGAND BINDING TO BETA-ADRENOCEPTORS

The biodistribution of S-(-)-4-(2-hydroxy-3-(1'-[ F-18]fluoroisopropyl )-aminopropoxy)carbazole ([F-18]S-fluorocarazolol, a nonselective beta -adrenoceptor antagonist) was studied in rats (60 min after F-18 injec tion when specific binding in peripheral organs was maximal). F-18 upt ake in brain, erythrocytes, heart and lung appeared to be linked to be ta-adrenoceptors. CGP-20712A and ICI-89,406 inhibited F-18 uptake in h eart (predominantly beta(1)-adrenoceptors) more potently than in lungs (predominantly beta(2)-adrenoceptors). In contrast, ICI-118,551 and p rocaterol were more potent in the lungs than in the heart. ICI-118,551 inhibited F-18 uptake in cerebellum (predominantly beta(2)-adrenocept ors) more potently than in cerebral cortex (predominantly beta(1)-adre noceptors). Stereoselectivity of the in vivo binding was demonstrated since S-(-)-propranolol inhibited uptake in target tissues more effect ively than R-(+)-propranolol. Myocardial and cerebral imaging may be h ampered by poor heart-to-lung contrast and low signal-to-noise ratios, but [F-18]S-fluorocarazolol seems suitable for positron emission tomo graphy (PET) of pulmonary beta-adrenoceptors.