Kinetic model for the fate of 6-[18F]fluorodopamine in the human heart: a novel means to examine cardiac sympathetic neuronal function
dc.contributor.author | Linares, Oscar | en_US |
dc.contributor.author | Kopin, Irwin J. | en_US |
dc.contributor.author | Katzper, Meyer | en_US |
dc.contributor.author | Goldstein, David S. | en_US |
dc.date.accessioned | 2006-09-08T19:48:47Z | |
dc.date.available | 2006-09-08T19:48:47Z | |
dc.date.issued | 2002-01 | en_US |
dc.identifier.citation | Goldstein, David S.; Katzper, Meyer; Linares, Oscar; Kopin, Irwin J.; (2002). "Kinetic model for the fate of 6-[18F]fluorodopamine in the human heart: a novel means to examine cardiac sympathetic neuronal function." Naunyn-Schmiedeberg's Archives of Pharmacology 365(1): 38-49. <http://hdl.handle.net/2027.42/41952> | en_US |
dc.identifier.issn | 0028-1298 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/41952 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=11862332&dopt=citation | en_US |
dc.description.abstract | After injection of 6-[ 18 F]fluorodopamine, thoracic positron emission tomographic scanning visualizes the sympathetic innervation of the heart. This report introduces a kinetic model that relates 6-[ 18 F]fluorodopamine positron emission tomographic scanning results to specific aspects of cardiac sympathoneural function. Inputs were the 6-[ 18 F]fluorodopamine concentration in arterial blood and the estimated contribution of circulating metabolites of 6-[ 18 F]fluorodopamine. All of the three compartments in the model were intraneuronal. Two compartments corresponded to vesicles in sympathetic nerves, consistent with the "multiple vesicular pool" hypothesis from preclinical studies. The model successfully fit the empirical time-activity curve for myocardial 6-[ 18 F]fluorodopamine-derived radioactivity and predicted correctly the effects of several neuropharmacological and physiological manipulations on the time-activity curve. Myocardial cell uptake of metabolites of 6-[ 18 F]fluorodopamine from the circulation could explain an immediate peak of 6-[ 18 F]fluorodopamine-derived radioactivity. The model seems useful in predicting effects of altered cardiac sympathetic function on time-activity curves for myocardial 6-[ 18 F]fluorodopamine-derived radioactivity in humans. | en_US |
dc.format.extent | 200074 bytes | |
dc.format.extent | 3115 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Springer-Verlag | en_US |
dc.subject.other | Positron Fluorodopamine Sympathetic Norepinephrine Modeling | en_US |
dc.subject.other | Legacy | en_US |
dc.title | Kinetic model for the fate of 6-[18F]fluorodopamine in the human heart: a novel means to examine cardiac sympathetic neuronal function | en_US |
dc.type | Article | en_US |
dc.subject.hlbsecondlevel | Pharmacy and Pharmacology | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | University of Michigan, Ann Arbor, Michigan, USA, | en_US |
dc.contributor.affiliationother | Clinical Neurocardiology Section, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland, USA, | en_US |
dc.contributor.affiliationother | Center for Drug Evaluation and Research, Food and Drug Administration, Rockville, Maryland, USA, | en_US |
dc.contributor.affiliationother | Clinical Neurocardiology Section, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland, USA, | en_US |
dc.contributor.affiliationumcampus | Ann Arbor | en_US |
dc.identifier.pmid | 11862332 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/41952/1/210-365-1-38_s002100100426.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1007/s002100100426 | en_US |
dc.identifier.source | Naunyn-Schmiedeberg's Archives of Pharmacology | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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