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Pulmonary oxygen toxicity: Demonstration of abnormal capillary permeability using contrast-enhanced MRI
Authors:R C Brasch  Y Berthezène  V Vexler  W Rosenau  O Clément  A Mühler  R Kuwatsuru  D M Shames
Institution:(1) Contrast Media Laboratory, Department of Radiology, University of California, 513 Parnassus Avenue, 94143-0628 San Francisco, CA, USA;(2) Contrast Media Laboratory, Department of Pathoanatomy, University of California, San Francisco, CA, USA
Abstract:An animal model of oxygen-induced pulmonary injury was used to assess the potential of contrastenhanced MRI to identify and quantify abnormal capillary permeability. Sprague-Dawley rats were exposed to 100% oxygen for 48 h (n=5) or 60 h (n=9). Axial spinecho MR images were acquired in intubated, anesthetized rats with ECG-gating (TR 400; TE 6) immediately or 7 days after the cessation of oxygen exposure. Polylysine-Gd-DTPA, a macromolecular paramagnetic blood-pool marker, was then given intravenously and the lungs were serially imaged for 42 to 47 min to monitor changes in signal intensity. Pulmonary enhancement was stable in rats exposed to 48 h of oxygen, and in rats exposed to 60 h of oxygen and given 7 days to recover. However, animals exposed to 100% oxygen for 60 h without a period of recovery showed a progressive increase in lung signal intensity for 15 min after polylysine-Gd-DTPA. Pleural effusions also showed progressively increasing signal, reflecting a capillary endothelial leak. A two compartment model describing the kinetics of polylysine-Gd-DTPA in the plasma and interstitial water of the lung was consistent with the dynamic MRI data and allowed estimation of the fractional leak rate (0.235 min–1) of the contrast agent from plasma to interstitial water. Given the assumption of our kinetic model, MRI following intravenous administration of polylysine-Gd-DTPA can be used to quantitate changes in capillary integrity induced by hyperoxia, including acute capillary leakiness and return to normal endothelial integrity with recovery from hyperoxic injury.This study was supported in part by CA 49786 from the National Cancer Institute. Y.B. was supported in part by Bourse de Recherche Scientifique et Technique du Traite de l'Atlantique Nord (O.T.A.N.)Presented at the 1992 Annual Meeting of the Society for Pediatric Radiology in Orlando, Florida; recipient of the Caffey Award
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