The evolution of isolated bilateral lung contusion from blunt chest trauma in rats : Cellular and cytokine responses

Lung contusion is the leading cause of death from blunt thoracic trauma in adults, but its mechanistic pathophysiology remains unclear. This study uses a recently developed rat model to investigate the evolution of inflammation and injury in isolated lung contusion. Bilateral lung contusion with min...

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Published in:	Shock (Augusta, Ga.) Vol. 24; no. 2; pp. 132 - 138
Main Authors:	RAGHAVENDRAN, Krishnan, DAVIDSON, Bruce A, WOYTASH, James A, HELINSKI, Jadwiga D, MARSCHKE, Cristi J, MANDERSCHEID, Patricia A, NOTTER, Robert H, KNIGH, Paul R
Format:	Journal Article
Language:	English
Published:	Augusta, GA BioMedical Press 01-08-2005
Subjects:	Albumins - metabolism Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Animals Biological and medical sciences Blood Pressure Bronchiolitis Obliterans - metabolism Bronchoalveolar Lavage Fluid Chemokine CCL2 - metabolism Chemokine CCL8 Chemokine CXCL2 Chemokines, CXC - metabolism Contusions - metabolism Cytokines - metabolism Fibrosis - metabolism Hemorrhage - pathology Hypoxia Inflammation Injuries of the thorax. Foreign bodies. Diseases due to physical agents Intensive care medicine Intercellular Signaling Peptides and Proteins - metabolism Interleukin-1 - metabolism Interleukin-6 - metabolism Investigative techniques, diagnostic techniques (general aspects) Lung - pathology Lung Injury Medical sciences Monocyte Chemoattractant Proteins - metabolism Monokines - metabolism Neutropenia - drug therapy Neutrophils - drug effects Neutrophils - metabolism Oxygen - metabolism Pneumonia - metabolism Pressure Radiodiagnosis. Nmr imagery. Nmr spectrometry Rats Respiratory system Thoracic Injuries - metabolism Time Factors Traumas. Diseases due to physical agents Vinblastine - pharmacology Wounds, Nonpenetrating Animal model Lung disease Oxygen Intensive care Rat Respiratory disease Rodentia Cytokine Contusion Trauma acute lung injury Vertebrata Mammalia Animal Evolution Hypoxia Lung contusion Resuscitation blunt trauma
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Summary:	Lung contusion is the leading cause of death from blunt thoracic trauma in adults, but its mechanistic pathophysiology remains unclear. This study uses a recently developed rat model to investigate the evolution of inflammation and injury in isolated lung contusion. Bilateral lung contusion with minimal cardiac trauma was induced in 54 anesthetized rats by dropping a 0.3-kg hollow cylindrical weight onto a precordial shield (impact energy, 2.45 Joules). Arterial oxygenation, pressure-volume (P-V) mechanics, histology, and levels of erythrocytes, leukocytes, albumin, and inflammatory mediators in bronchoalveolar lavage (BAL) were assessed at 8 min, at 4, 12, 24, and 48 h, and at 7 days after injury. The role of neutrophils in the evolution of inflammatory injury was also specifically studied by depleting these cells with intravenous vinblastine before lung contusion. Arterial oxygenation was severely reduced at 8 min to 24 h postcontusion, but became almost normal by 48 h. Levels of erythrocytes, leukocytes, and albumin in BAL were increased at <or=24 h, and returned toward normal by 48 h. Deficits in P-V mechanics were most apparent at 24 h postcontusion. Levels of macrophage inflammatory polypeptide-2, cytokine-induced neutrophil chemoattractant-1, and interleukin 6 in BAL peaked at 24 h, whereas monocyte chemoattractant protein-1 and interleukin 1beta peaked at 24 to 48 h postcontusion. Histology showed early hemorrhagic injury (8 min-12 h), with neutrophilic infiltration at 24 h and areas of bronchiolitis obliterans organizing pneumonia-associated fibrosis at 7 days. Vinblastine-treated neutropenic rats had significantly reduced lung injury based on total lung volume at 4 h and on BAL albumin levels at 24 h postcontusion. Inflammatory injury from isolated bilateral lung contusion in rats is most severe in the acute period (8 min-24 h) after initial blunt trauma, and includes a component of neutrophil-dependent pathology.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	1073-2322 1540-0514
DOI:	10.1097/01.shk.0000169725.80068.4a