Faculty Collaboration Database

Lung tissue mitochondrial benzodiazepine receptors increase in a model of pulmonary inflammation. Lung 2002;180(5):241-50

Date

12/19/2002

Pubmed ID

12489018

DOI

10.1007/s004080000098

Scopus ID

2-s2.0-0036364533 (requires institutional sign-in at Scopus site)   10 Citations

Abstract

Pulmonary inflammation induced in the rabbit lung by the intravenous injection of complete Freund's adjuvant (CFA) increases the lung uptake of 14C-diazepam from the pulmonary circulation. The objective of this study was to determine the extent to which mitochondrial (or peripheral) benzodiazepine receptors (mBRs) may contribute to this increased uptake. To this end, we measured the pulmonary venous effluent concentration versus time for 14C-diazepam following its injection into the pulmonary artery of isolated perfused normal and CFA inflamed lungs with and without an inhibitor (PK11195) of diazepam binding to mBRs. The results demonstrate that this model of pulmonary inflammation is associated with an increase in lung tissue mBR. Lung tissue caspase-3 activity was also measured as one index of lung inflammation, and we found that in inflamed lungs, there was an inverse correlation between mBR density and lung tissue capase-3 activity. This is consistent with observations in other organs and a role for mBRs in apoptotic elimination of inflammatory cells in the resolution of this inflammatory response. The results suggest the potential utility of mBR ligands for noninvasive detection and/or characterization of pulmonary inflammation, e.g., via nuclear medicine methods.

Author List

Audi SH, Dawson CA, Ahlf SB, Roerig DL

Author

Said Audi PhD Professor in the Biomedical Engineering department at Marquette University

MESH terms used to index this publication - Major topics in bold

Animals
Carbon Radioisotopes
Caspase 3
Caspases
Diazepam
Enzyme Precursors
Female
Freund's Adjuvant
Inflammation
Lung
Male
Rabbits
Receptors, GABA-A