Use of iodine-123 metaiodobenzylguanidine scintigraphy for the detection of amiodarone induced pulmonary toxicity in a rabbit model: a comparative study with technetium-99m diethyltriaminepenta acetic acid radioaerosol scintigraphy.

Department of Nuclear Medicine, Faculty of Medicine, Trakya University, Edirne, Turkey.
Annals of Nuclear Medicine (Impact Factor: 1.51). 06/2005; 19(3):217-24. DOI: 10.1007/BF02984608
Source: PubMed

ABSTRACT The purpose of the study was; (i) to determine whether 123I-MIBG scintigraphy is sensitive for detection of amiodarone induced pulmonary toxicity (AIPT) and (ii) to compare it with 99mTc-DTPA radioaerosol. Twelve white New Zealand rabbit with initial mean body weight 4.24 +/- 0.47 g were divided into two groups. AIPT group (n = 7) was administered amiodarone (20 mg/kg BW). The control group (n = 5) received the same amount of 0.9% saline. All animals underwent 123I-MIBG and 99mTc-DTPA radioaerosol scintigraphy at the end of the treatment period. 123I-MIBG static thorax images were obtained during 10 minutes at 15 minutes and 3-hours after intravenous injection of the radiopharmaceutical. Lung to heart ratios (LHR) and lung to mediastinum ratios (LMR), and retention index (LRI) of 123I-MIBG were determined. Two days after 123I-MIBG scintigraphy, 99mTc-DTPA radioaerosol scintigraphy was performed, and clearance from the lungs was measured for 10 min (1 min/frame) following termination of inhalation. 123I-MIBG lung retention index (LRI) was significantly higher in the AIPT group than the control (61 +/- 4.6 vs. 40 +/- 4.5, p = 0.01). Early LHR and LMR were significantly lower in the AIPT group than in the control group (p = 0.04, p = 0.01, respectively), whereas those of late LHR and LMR were not significantly different. T1/2 values of DTPA clearance were significantly increased in AIPT group according to the control group (55 +/- 7.2 vs. 86.6 +/- 18.5, p = 0.02). 123I-MIBG scintigraphy is a valuable tool for detecting AIPT in a rabbit model. Additionally, 99mTc-DTPA radioaerosol scintigraphy is an excellent comprehensive investigational tool for detecting AIPT with the added advantage of lower cost.

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    ABSTRACT: Nuclear medicine techniques have the capacity to investigate neuronal dysfunction at the synapse level. For instance, metaiodobenzylguanidine (MIBG) shows a similar uptake, storage and release as norepinephrine. Intravenously injected radiolabeled MIBG is able to reflect neuronal damage induced by inflammation and tumors. The purpose of this review is to evaluate the results and the limitation of these neuronal imaging techniques in patients with pulmonary and cardiac diseases and to give an opinion about the clinical value of these new diagnostic tools. MIBG neuronal images of the lungs and heart can show heterogeneous distribution patterns with either diminished or increased MIBG uptake and/or washout. These changes reflect changes in endothelial integrity, neuronal innervations and clearance of norepinephrine. Interest in the role of neurotransmitter involvement and the relation between endothelial cell integrity and vascularization is growing and of utmost importance to understand the effect on pathophysiology of diseases. At this moment, there is no added clinical value to routinely use MIBG scanning of the lungs and the heart. This is partly due to the many unresolved questions such as what actually happens and which factors influence MIBG uptake and washout under normal physiological circumstances. But the technique, if standardized and when dynamic time acquisition is performed with the latest equipment, such as PET and single photon emission computed tomography-computed tomography (SPECT-CT), has a tremendous potential. It can unravel upto now unknown relationships between innervation, vascularization and endothelial integrity. Other diagnostic tools such as MRI and CT do not have this capacity, so the future looks bright for these new neuronal imaging techniques.
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    ABSTRACT: Introduction: Amiodarone is gaining support as a first-line antiarrhythmic drug despite its potentially fatal pulmonary complications involving inflammation and fibrosis. Objective: This study was undertaken to investigate the effect of long-term amiodarone administration and withdrawal on the histological structure of rat lung. In addition, the possible protective role of vitamin E supplementation was studied. Materials and methods: This study was carried out on 36 adult male albino rats, which were divided into four groups: group I, which was considered as control; group II (amiodarone-treated group), which received amiodarone orally in a daily dose of 30 mg/kg body weight for 12 weeks; group III (withdrawal group), which received the same dose of amiodarone for 12 weeks and were sacrificed 6 weeks after withdrawal of the drug; and group IV (protected group), which received vitamin E orally in a daily dose of 100 mg/kg body weight simultaneously with amiodarone for 12 weeks. At the time of sacrifice, the lungs were dissected and tissue samples were processed for both light and electron microscopic studies. Immuohistochemical study using anti-CD68 for showing alveolar macrophages was also performed and the number of positively stained cells was morphometrically estimated and statistically analyzed. Results: Administration of amiodarone alone showed an alteration in the lung architecture in the form of collapsed alveoli with evident proliferation and vacuolation of pneumocytes type II. Thickening of interalveolar septa, cellular infiltration, and collagen deposition associated with an increased number of macrophages as proved by the morphometric study were demonstrated. Intrabronchial cellular debris and vascular congestion were also observed. Coadministration of amiodarone with vitamin E showed a considerable degree of preservation of the pulmonary alveolar architecture; however, a mild improvement in the lung injury was observed in animals after amiodarone withdrawal. The alveoli were lined mainly by vacuolated pneumocytes type II with moderately thickened interalveolar septa. Conclusion: From this study it could be concluded that prolonged administration of amiodarone in rats can induce severe lung damage. Withdrawal of the drug showed little improvement of this harmful effect but concomitant administration of vitamin E effectively protected the lung tissue. In addition, the increased number of alveolar macrophages associated with amiodarone administration has supported the concept that these cells may play a role in the pathogenesis of lung injury caused by amiodarone.
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