title: Physiologic basis of pulmonary edema during intestinal reperfusion.
abstract: This study quantitates the physiologic forces governing the movement of fluid and protein into the lungs during intestinal reperfusion (IR) and describes the anatomic pattern of protein extravasation. Sprague-Dawley rats underwent IR after which pulmonary microvascular dysfunction was assessed in vivo by measuring the concentration of protein within the airways and by quantitating the extravasation of Evans blue dye (EBD). Pulmonary microvascular dysfunction was quantitated in vitro by determining the capillary filtration coefficient (Kf), protein reflection coefficient (final sigma), and vascular resistance (Rt) using an isolated, perfused lung model. The morphologic pattern of protein extravasation into the lung was qualitatively assessed by fluorescence microscopy following the intravenous administration of fluorescent-labeled proteins of varying molecular weight. Sham-operated animals served as controls. The EBD content of lungs of IR animals was 48% greater than that of controls (P = 0.02). There was no difference in the protein concentration within the airways of these two groups. IR was associated with changes in pulmonary microvascular function favoring the movement of plasma fluid and protein into the interstitium (Kf = 0.02 +/- 0.006 vs 0.005 +/- 0.0005 g/min/mm Hg/100 g body wt; final sigma = 0.95 +/- 0.02 vs 0.99 +/- 0.005; and Rt = 0.94 +/- 0.08 vs 0. 53 +/- 0.04 mm Hg/ml/min/100 g body wt; IR vs SHAM, respectively, P < 0.05). Fluorescence microscopy demonstrated the focal extravasation of labeled proteins into the lungs of animals sustaining IR. These data suggest that both enhanced microvascular permeability and increased hydrostatic pressure contribute to the pulmonary edema associated with IR. Furthermore, the extravasation of protein is relatively focal in nature in contrast to the diffuse leak that characterizes more severe models of lung injury.
authors.affiliation: Department of Surgery, University of Texas Southwestern Medical School, Dallas, Texas, USA.
authors.forename: J L
authors.initials: JL
authors.lastname: Iglesias
authors.forename: J L
authors.initials: JL
authors.lastname: LaNoue
authors.forename: T E
authors.initials: TE
authors.lastname: Rogers
authors.forename: L
authors.initials: L
authors.lastname: Inman
authors.forename: R H
authors.initials: RH
authors.lastname: Turnage
mesh_terms: D000818:Animals; D001826:Body Fluids / Q000378:metabolism; D004195:Disease Models, Animal; D066298:In Vitro Techniques; D007422:Intestines / Q000098:blood supply* / Q000293:injuries*; D008168:Lung / Q000473:pathology / Q000503:physiopathology; D055370:Lung Injury; D008297:Male; D008833:Microcirculation / Q000503:physiopathology; D008856:Microscopy, Fluorescence; D010477:Perfusion; D011506:Proteins / Q000378:metabolism; D011652:Pulmonary Circulation / Q000502:physiology; D011654:Pulmonary Edema / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000150:complications* / Q000473:pathology / Q000503:physiopathology
chemical_list: D011506:Proteins