Orthopedic Trauma-Induced Pulmonary Injury in the Obese Zucker Rat

Authors


Address for correspondence: Lusha Xiang, M.D., Department of Physiology and Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216-4505, USA. E-mail: lxiang2@physiology.umsmed.edu

Abstract

Please cite this paper as: Xiang, Hester, Fuller, Sebai, Mittwede, Jones, Aneja and Russell (2010). Orthopedic Trauma-Induced Pulmonary Injury in the Obese Zucker Rats. Microcirculation17(8), 650–659.

Abstract

Objective:  Obese subjects with orthopedic trauma exhibit increased inflammation and an increased risk of pulmonary edema. Prostaglandin E2 (PGE2) production is elevated during inflammation and associated with increased vascular permeability. We hypothesize that pulmonary edema in obesity following orthopedic trauma is due to elevated PGE2 and resultant increases in pulmonary permeability.

Methods:  Orthopedic trauma was induced in both hindlimbs in lean (LZ) and obese Zucker rats (OZ). On the following day, plasma interleukin-6 (IL-6) and PGE2 levels, pulmonary edema, and pulmonary gas exchange capability were compared between groups: LZ, OZ, LZ with trauma (LZT), and OZ with trauma (OZT). Vascular permeability in isolated lungs was measured in LZ and OZ before and after application of PGE2.

Results:  As compared with the other groups, the OZT exhibited elevated plasma IL-6 and PGE2 levels, increased lung wet/dry weight ratio and bronchoalveolar protein concentration, and an impaired pulmonary gas exchange. Indomethacin treatment normalized plasma PGE2 levels and pulmonary edema. Basal pulmonary permeability in isolated lungs was higher in OZ than LZ, with a further increase in permeability following treatment with PGE2.

Conclusions:  These results suggest that pulmonary edema in OZ following orthopedic trauma is due to an elevated PGE2 and resultant increases in pulmonary permeability.

Ancillary