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Minimally Invasive Techniques |

Positron Emission Tomography Studies of Human Airways Using an Inhaled β-Adrenoceptor Antagonist, S-11C-CGP 12388*

Aren van Waarde, PhD; Bram Maas, BSc; Petra Doze, PhD; Riemer H. Slart, MD; Henderik W. Frijlink, PhD; Willem Vaalburg, PhD; Philip H. Elsinga, PhD
Author and Funding Information

*From the Department of Nuclear Medicine & Molecular Imaging (Drs. Van Waarde, Doze, Slart, Vaalburg, and Elsinga, and Mr. Maas), University Medical Center of Groningen, the Netherlands; and the Department of Pharmaceutical Technology and Biopharmacy (Dr. Frijlink), Groningen University Institute for Drug Exploration (GUIDE), Groningen, the Netherlands.

Correspondence to: Aren van Waarde, PhD, Groningen University Medical Center, PO Box 30001, 9700RB Groningen, the Netherlands; e-mail: a.van.waarde@pet.azg.nl



Chest. 2005;128(4):3020-3027. doi:10.1378/chest.128.4.3020
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Objectives: Positron emission tomography (PET) scanning may provide information on changes in the density and affinity of airway β-adrenoceptors in lung diseases. However, the injection of a radiolabeled β-blocker results in a pulmonary PET signal that reflects the binding of the ligand in the alveoli and not in the airways. Better discrimination between alveolar and airway β-adrenoceptors may be possible with an inhaled radioligand.

Design: A nebulizer was used to administer the antagonist S-11C-CGP12388 in aerosol form. Eight volunteers inhaled the tracer twice, at baseline and after pretreatment with a β-adrenergic drug. In both PET scan studies, a dynamic scan of the lungs was followed by a whole-body scan to assess the inhaled dose. Pulmonary uptake was quantified using a region-of-interest-based analysis.

Setting: University hospital.

Participants: Healthy volunteers.

Interventions: Pretreatment consisted either of inhaled salbutamol (400 μg, 20 min before the scan), or orally administered pindolol (3 × 5 mg during a period of 16 h before PET scanning).

Results: Drug pretreatment did not affect pulmonary deposition of the radioligand. The agonist salbutamol accelerated the monoexponential washout of 11C not only in the peripheral lung (mainly alveoli), but also in the central lung (mainly airways) and in the main bronchi. An even larger increase of the washout rate was induced by the antagonist pindolol.

Conclusion: The similar effects of pindolol and salbutamol on tracer kinetics suggest that accelerated washout is due to the blockade of β-adrenoceptors. Thus, the interaction of drugs with airway β-adrenoceptors can be visualized using PET scanning and an inhaled radioligand.

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