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Shock tubes have been extensively used in the study of blast traumatic brain injury due to increased incidence of blast-induced neurotrauma in Iraq and Afghanistan conflicts. One of the important aspects in these studies is how to best replicate the field conditions in the laboratory which relies on reproducing blast wave profiles. Evolution of the blast wave profiles along the length of the compression-driven air shock tube is studied using experiments and numerical simulations with emphasis on the shape and magnitude of pressure time profiles. In order to measure dynamic pressures of the blast, a series of sensors are mounted on a cylindrical specimen normal to the flow direction. Our results indicate that the blast wave loading is significantly different for locations inside and outside of the shock tube. Pressure profiles inside the shock tube follow the Friedlander waveform fairly well. Upon approaching exit of the shock tube, an expansion wave released from the shock tube edges significantly degrades the pressure profiles. For tests outside the shock tube, peak pressure and total impulse reduce drastically as we move away from the exit and majority of loading is in the form of subsonic jet wind. In addition, the planarity of the blast wave degrades as blast wave evolves three dimensionally. Numerical results visually and quantitatively confirm the presence of vortices, jet wind and three-dimensional expansion of the planar blast wave near the exit. Pressure profiles at 90° orientation show flow separation. When cylinder is placed inside, this flow separation is not sustained, but when placed outside the shock tube this flow separation is sustained which causes tensile loading on the sides of the cylinder. Friedlander waves formed due to field explosives in the intermediate-to far-field ranges are replicated in a narrow test region located deep inside the shock tube.

We evaluated the acute (up to 24 h) pathophysiological response to primary blast using a rat model and helium driven shock tube. The shock tube generates animal loadings with controlled pure primary blast parameters over a wide range and field-relevant conditions. We studied the biomechanical loading with a set of pressure gauges mounted on the surface of the nose, in the cranial space, and in the thoracic cavity of cadaver rats. Anesthetized rats were exposed to a single blast at precisely controlled five peak overpressures over a wide range (130, 190, 230, 250, and 290 kPa). We observed 0% mortality rates in 130 and 230 kPa groups, and 30%, 24%, and 100% mortality rates in 190, 250, and 290 kPa groups, respectively. The body weight loss was statistically significant in 190 and 250 kPa groups 24 h after exposure. The data analysis showed the magnitude of peak-to-peak amplitude of intracranial pressure (ICP) fluctuations correlates well with mortality rates. The ICP oscillations recorded for 190, 250, and 290 kPa are characterized by higher frequency (10-20 kHz) than in other two groups (7-8 kHz). We noted acute bradycardia and lung hemorrhage in all groups of rats subjected to the blast. We established the onset of both corresponds to 110 kPa peak overpressure. The immunostaining against immunoglobulin G (IgG) of brain sections of rats sacrificed 24-h post-exposure indicated the diffuse blood-brain barrier breakdown in the brain parenchyma. At high blast intensities (peak overpressure of 190 kPa or more), the IgG uptake by neurons was evident, but there was no evidence of neurodegeneration after 24 h post-exposure, as indicated by cupric silver staining. We observed that the acute response as well as mortality is a non-linear function over the peak overpressure and impulse ranges explored in this work.