Cardiopulmonary, histological and inflammatory alterations after lung contusion in a novel mouse model of blunt chest trauma.: Reply:

We would like to thank Dr. Guy and Dr. Watkins for their letter and their comments regarding our recently published paper describing a novel mouse model of blunt chest trauma in mice. We also thank the Editors of Shock for the opportunity to respond to this letter. In our experiments, blunt chest trauma was induced using a single blast wave of high intensity centered on the thorax of male C3H/HeN mice. Blast pressure was measured directly at the nozzle of the blast wave generator to assess reproducibility of the blast wave released. The pressure was not determined at the animal's chest because we feel that measuring the intensity of the blast wave that impacts the animal is less informative than biological parameters. Thus, among other measurements, the degree and distribution of lung hemorrhage was estimated macroscopically and microscopically to characterize the trauma. Assessing the distribution of hemorrhage was considered important to monitor whether the trauma consistently caused a bilateral lung contusion. Dr. Guy's and Dr. Watkins' suggestion to determine lung weight ratio and the injury quotient in this model is excellent and will be addressed in future studies. We certainly agree that the observed increase in plasma cytokine concentrations at 3 h following blunt chest trauma is not sufficient to characterize the immunologic response to the trauma, although it suggests a systemic response. As a first step in a series of experiments it was the primary goal of our studies to develop a model of blunt chest trauma in mice because this species is particularly suitable for detailed immunologic investigations. Ongoing work proves that this model is appropriate for such studies and focuses on cell-mediated immune responses and their changes over time. The comments about liver injury are very interesting. Macroscopic as well as microscopic analysis did not reveal significant liver injury at the early time point used in our experiments. In addition, measurement of myeloperoxidase activity in liver tissue did not show any differences between sham and trauma animals, although marked differences occurred in the lungs. An explanation might be that the blast wave primarily affects air-containing structures and was exactly focused on the thorax. During preliminary experiments, however, damage to the liver was observed when the focus of the blast wave was centered too close to the abdomen. Thus, we agree that blunt chest trauma in this model might to some extent have impact on the liver. In this regard, indirect effects of passive downward movement of the diaphragm or deformation of the thorax appear possible. We therefore think that this model should be considered as a model of blunt chest trauma that mimics blunt chest injury as it occurs clinically and includes all pathophysiological components. However, because no fractures occur and collateral injury to soft tissue and abdominal organs is almost absent, we are convinced that the model makes it possible to study the effects of severe bilateral lung contusion. Dr. Markus Knöferl

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