A Rat Model for Isolated Bilateral Lung Contusion from Blunt Chest Trauma

Abstract

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 (1.8-2.7 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 < or =24 h, improving by 48 h. BAL albumin levels were highest at < or =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.

The role of thoracic trauma in inflammatory responses, apoptosis and bacterial translocation following multipl trauma

“…This data suggests that additional processes should be investigated in order to clarify lung injury and causes of morbidity. [3][4][5] These studies also reported that TNF-α and IL-1ß were primary mediators in the activation of other cytokines, and ensured prostaglandin release, synthesis of pro-coagulant factors and activation of leukocyte chemotaxis with adhesion molecules like ICAM and E-selectin. Accumulation of neutrophils increases the production and release of vasoactive substances (leukotrienes, eicosanoids, platelet-activating factor) and proteolytic enzymes (elastase, cathepsin G).…”

“…The thoracic trauma groups (Group TT) were exposed to thoracic trauma using the mechanism published by Raghavendran et al with a force of 2.7 J followed by anesthesia. [4] In the head trauma groups (Group HT), severe head trauma was created according to the method described by Foda et al [11] Sequential thoracic and head traumas were created in the same manner as mentioned above in the groups receiving thoracic and head traumas (Group HTT). Twenty four or 48 hours after the trauma, the rats were anesthetized and the chest cavities were opened.…”

“…Furthermore, it was noted that apoptosis following thoracic traumas may be associated with the inflammatory response. [3][4][5][6] Bacterial translocation refers to the spread of bacteria and their products in the intestinal flora to solid organs, which can be due to intestinal hypoperfusion, burns and stress. Bacterial translocation has been cited as one of the leading factors in the development of acute lung injury, MOF and sepsis.…”

An Evaluation of The Systemic Antiinflammatory Effects of Levosimendan in Experimental Blunt Thoracic Trauma Model

“…[20] In the current study, because the results of the histopathological examination of pulmonary tissues obtained 6 h after the formation of blunt thorax trauma, which included alveolar hemorrhage, alveolar edema, and neutrophil infiltration, were similar to the those of the trauma model described by Raghavendran et al, the efficacy of the current study model was confirmed. [15] According to these results, PC model was successfully established in the rats. After analyzing the results obtained from the histopathological examination in this study, although a statistical difference was not observed, when the median values were examined, the high dose of levosimendan was considered to reduce alveolar hemorrhage that developed after trauma; however, when a low dose was administered, no effect on alveolar hemorrhage was observed.…”

“…1). [15] To reduce cardiac injury to a minimum and have a minimum effect on hemodynamic instability, the contusion was unilaterally induced to the right lung.…”