Anesth Analg 2005;101:1482-1489
© 2005 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000180201.25746.1F
CRITICAL CARE AND TRAUMA
A Rat Model for Isolated Bilateral Lung Contusion from Blunt Chest Trauma
Krishnan Raghavendran, MD* ,
Bruce A. Davidson, BS ,
Jadwiga D. Helinski, BS ,
Cristi J. Marschke ,
Patricia Manderscheid, PhD ,
James A. Woytash, MD ,
Robert H. Notter, MD, PhD , and
Paul R. Knight, MD, PhD
Departments of *Surgery, Anesthesiology, and Pathology, State University of New York (SUNY) at Buffalo, Buffalo; and Department of Pediatrics, University of Rochester, Rochester, New York
Address correspondence and reprint requests to Krishnan Raghavendran, MD, Department of Surgery (Division of Trauma and Critical Care), SUNY at Buffalo, David K. Miller Building, Suite 316, 462 Grider St., Suite 316, Buffalo, NY 14215. Address e-mail to kraghave{at}ecmc.edu.
Lung contusion affects 17%25% of adult blunt trauma patients, and is the leading cause of death from blunt thoracic injury. A small animal model for isolated bilateral lung contusion has not been developed. We induced lung contusion in anesthetized rats by dropping a 0.3-kg weight onto a precordial protective shield to direct the impact force away from the heart and toward the lungs. Lung injury was characterized as a function of chest impact energy (1.82.7 J) by measurements of arterial oxygenation, bronchoalveolar lavage (BAL) albumin and cytology, pressure-volume mechanics, and histopathology. Histology confirmed bilateral lung contusion without substantial cardiac muscle trauma. Rats receiving 2.7 J of chest impact energy had 33% mortality that exceeded prospectively defined limits for sublethal injury. Hypoxemia in rats with maximal sublethal injury (2.45 J) met criteria for acute lung injury at 24 h, improving by 48 h. BAL albumin levels were highest at 24 h, and remained elevated along with increased BAL leukocytes and decreased lung volumes at 48 h. We concluded that an impact energy of 2.45 J induces isolated, bilateral lung contusion and provides a useful model for future mechanistic pathophysiological assessments.
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S. Lakshminrusimha, B. A Davidson, R. M Ryan, J. D Helinski, and K. Raghavendran
Abstract 88: Alterations in Pulmonary Vasoreactivity Following Lung Contusion in Rats
Circulation,
October 31, 2007;
116(16_MeetingAbstracts):
II_942 - II_942.
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