Radiolabeled meta-iodobenzylguanidine and the adrenergic neurons of salivary glands

The handling of radiolabeled meta-iodobenzylguanidine (MIBG) by salivary glands was evaluated. In the submaxillary glands of rats, the uptake of 125I-MIBG was decreased after 1) nerve injury induced by 6-hydroxydopamine, 2) inhibition of the uptake-1 pathway by desmethylimipramine, and 3) surgical d...

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Published inAmerican journal of physiologic imaging Vol. 2; no. 1; p. 1
Main Authors Sisson, J C, Wieland, D M, Jaques, Jr, S, Sherman, P, Fisher, S, Mallette, S, Meyers, L, Mangner, T J
Format Journal Article
LanguageEnglish
Published Denmark 1987
Subjects
3-Iodobenzylguanidine
Adrenergic Fibers - metabolism
Adult
Animals
Female
Humans
Iodine Radioisotopes
Iodobenzenes - pharmacokinetics
Male
Middle Aged
Radionuclide Imaging
Rats
Rats, Inbred Strains
Salivary Glands - diagnostic imaging
Salivary Glands - innervation
Salivary Glands - metabolism
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Summary:The handling of radiolabeled meta-iodobenzylguanidine (MIBG) by salivary glands was evaluated. In the submaxillary glands of rats, the uptake of 125I-MIBG was decreased after 1) nerve injury induced by 6-hydroxydopamine, 2) inhibition of the uptake-1 pathway by desmethylimipramine, and 3) surgical denervation. However, the reduction in 125I-MIGB uptake was less than that of 3H-norepinephrine (3H-NE) and of the endogenous content of NE in the glands. Yet, the sympathomimetic phenylpropanolamine displaced about the same fraction of 125I-MIBG as 3H-NE. These results suggest that 40% or more of 125I-MIBG resides in extraneuronal sites but that at least 30% and possibly more lies in the adrenergic nerve terminals. Fasting and feeding rats produced changes in the rates of disappearance of 125I-MIBG and 3H-NE from the submaxillary gland that were different, and the rates of loss of 125I-MIBG cannot be used as an index of adrenergic nerve activity. In man, the concentrations of 123I-MIBG in the salivary glands, particularly the parotid gland, are readily visible and measureable. Imipramine reduced the uptake of 123I-MIBG into parotid glands little or not at all; some of the 123I-MIBG may enter neurons via an imipramine-insensitive pathway, but a substantial fraction probably arrives in intraneuronal locations. Thus, phenylpropanolamine displaced over 50% of the parotid pool of 123I-MIBG. However, in only the most severe case of generalized autonomic neuropathy was the uptake of 123I-MIBG reduced.
ISSN:0885-8276