Soft-armor Vest Effectiveness and Intrathoracic Biomechanics in Rodents Exposed to Primary Blast.

The biomechanics and efficacy of personal protective equipment in mitigating injuries from blast overpressure remain unclear. The objectives of this study were to define intrathoracic pressures in response to blast wave (BW) exposure and biomechanically evaluate a soft-armor vest (SA) at diminishing these perturbations. Male Sprague-Dawley rats were instrumented with pressure sensors in the thorax and were exposed laterally to multiple exposures ranging from 33 to 108 kPa BW with SA and without SA. There were significant increases in rise time, peak negative pressure, and negative impulse in the thoracic cavity compared to the BW. Esophageal measurements were increased to a greater extent when compared to the carotid and the BW for all parameters (except positive impulse, which decreased). SA minimally altered the pressure parameters and energy content. This study establishes the relationship of external blast flow conditions and intra-body biomechanical responses in the thoracic cavity of rodents with and without SA.

A temporal evaluation of cytokines in rats after blast exposure.

Blast induced neurotrauma (BINT) has been a challenge clinically due to the associated diagnostic issues, overlapping symptoms with other forms of trauma, and delayed onset of the symptoms. Little is understood about the pathophysiology of BINT and there are no validated biomarkers available for diagnosis. Animal studies have shown elevated levels of inflammation in the brain after BINT using histological techniques. To identify key inflammatory biomarkers associated with BINT, cytokine microarrays were conducted. Male Sprague Dawley rats were exposed to a blast peak overpressure of 117kPa after anesthesia; control animals did not undergo blast exposure. Serum was collected at the designated sacrificed time which was either at 3, 24, 48, or 72 hours following blast exposure. We analyzed cytokines IL-1a, IL-1ß, TNF-a, IL-6, IL-10, Erythropoietin (EPO), macrophage colony stimulating factor (m-CSF), and Vascular Endothelial Growth Factor (VEGF). Results indicated a significant decrease of IL-1a at 3 hours, a decrease of m-CSF at 24 hours, an increase of EPO at 48 hours, decreased levels of IL-1a, IL-1ß, IL-6, IL-10, EPO, and increased levels of VEGF and m-CSF at 72 hours post blast. We found no changes in TNF-a at any time point. Collectively, the data suggest there is a compromised inflammatory response. Furthermore, the late decrease of EPO and increase of m-CSF indicated a delayed macrophage response to the ongoing inflammatory crisis. Overall, the results of the serum cytokine measurements following blast exposure signified a delayed inflammatory response.