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A Multiscale Approach to Blast Neurotrauma Modeling: Part II: Methodology for Inducing Blast Injury to in vitro Models.

Effgen GB, Hue CD, Vogel E, Panzer MB, Meaney DF, Bass CR, Morrison B - Front Neurol (2012)

Bottom Line: Blast-induced traumatic brain injury (bTBI) results from the translation of a shock wave in-air, such as that produced by an IED, into a pressure wave within the skull-brain complex.To better prevent and treat bTBI, both the initiating biomechanics and the ensuing pathobiology must be understood in greater detail.A well-characterized, in vitro model of bTBI, in conjunction with animal models, will be a powerful tool for developing strategies to mitigate the risks of bTBI.

View Article: PubMed Central - PubMed

Affiliation: Department of Biomedical Engineering, Columbia University New York, NY, USA.

ABSTRACT
Due to the prominent role of improvised explosive devices (IEDs) in wounding patterns of U.S. war-fighters in Iraq and Afghanistan, blast injury has risen to a new level of importance and is recognized to be a major cause of injuries to the brain. However, an injury risk-function for microscopic, macroscopic, behavioral, and neurological deficits has yet to be defined. While operational blast injuries can be very complex and thus difficult to analyze, a simplified blast injury model would facilitate studies correlating biological outcomes with blast biomechanics to define tolerance criteria. Blast-induced traumatic brain injury (bTBI) results from the translation of a shock wave in-air, such as that produced by an IED, into a pressure wave within the skull-brain complex. Our blast injury methodology recapitulates this phenomenon in vitro, allowing for control of the injury biomechanics via a compressed-gas shock tube used in conjunction with a custom-designed, fluid-filled receiver that contains the living culture. The receiver converts the air shock wave into a fast-rising pressure transient with minimal reflections, mimicking the intracranial pressure history in blast. We have developed an organotypic hippocampal slice culture model that exhibits cell death when exposed to a 530 ± 17.7-kPa peak overpressure with a 1.026 ± 0.017-ms duration and 190 ± 10.7 kPa-ms impulse in-air. We have also injured a simplified in vitro model of the blood-brain barrier, which exhibits disrupted integrity immediately following exposure to 581 ± 10.0 kPa peak overpressure with a 1.067 ± 0.006-ms duration and 222 ± 6.9 kPa-ms impulse in-air. To better prevent and treat bTBI, both the initiating biomechanics and the ensuing pathobiology must be understood in greater detail. A well-characterized, in vitro model of bTBI, in conjunction with animal models, will be a powerful tool for developing strategies to mitigate the risks of bTBI.

No MeSH data available.


Related in: MedlinePlus

Characterization of the open shock tube. (A) Three in-air pressure transducers located equidistant around the exit to the shock tube recorded pressure transients in-air for blast of a 1.5-mm thick PET burst membrane. The peak overpressure [denoted by point (C)] for this blast was 534 kPa with a duration of 1.040 ms and an impulse of 184 kPa-ms. (B) The output of the shock tube was similar in shape to the Friedlander wave, which models the primary blast produced from an explosion in the free-field. (C) For the open shock tube, the durations were plotted as a function of the peak overpressures for each blast and fit to a second-order polynomial (n = 78). (D) For the open tube, the impulses were plotted as a function of peak overpressures for each blast and fit to a second-order polynomial (n = 78).
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Figure 2: Characterization of the open shock tube. (A) Three in-air pressure transducers located equidistant around the exit to the shock tube recorded pressure transients in-air for blast of a 1.5-mm thick PET burst membrane. The peak overpressure [denoted by point (C)] for this blast was 534 kPa with a duration of 1.040 ms and an impulse of 184 kPa-ms. (B) The output of the shock tube was similar in shape to the Friedlander wave, which models the primary blast produced from an explosion in the free-field. (C) For the open shock tube, the durations were plotted as a function of the peak overpressures for each blast and fit to a second-order polynomial (n = 78). (D) For the open tube, the impulses were plotted as a function of peak overpressures for each blast and fit to a second-order polynomial (n = 78).

Mentions: Characterization of the shock tube was performed without the receiver in place (Figure 2). Pressure time-histories recorded at the end of the shock tube were typical of a Friedlander wave (Figure 2B) and demonstrated good inter-test consistency (Figure 2A). Duration of the positive pressure phase was correlated with peak overpressure, and the relationship was well-defined by a second-order polynomial fit (Figure 2C). The impulse was also correlated with peak overpressure and was well-defined by a second-order polynomial as well (Figure 2D).


A Multiscale Approach to Blast Neurotrauma Modeling: Part II: Methodology for Inducing Blast Injury to in vitro Models.

Effgen GB, Hue CD, Vogel E, Panzer MB, Meaney DF, Bass CR, Morrison B - Front Neurol (2012)

Characterization of the open shock tube. (A) Three in-air pressure transducers located equidistant around the exit to the shock tube recorded pressure transients in-air for blast of a 1.5-mm thick PET burst membrane. The peak overpressure [denoted by point (C)] for this blast was 534 kPa with a duration of 1.040 ms and an impulse of 184 kPa-ms. (B) The output of the shock tube was similar in shape to the Friedlander wave, which models the primary blast produced from an explosion in the free-field. (C) For the open shock tube, the durations were plotted as a function of the peak overpressures for each blast and fit to a second-order polynomial (n = 78). (D) For the open tube, the impulses were plotted as a function of peak overpressures for each blast and fit to a second-order polynomial (n = 78).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3285773&req=5

Figure 2: Characterization of the open shock tube. (A) Three in-air pressure transducers located equidistant around the exit to the shock tube recorded pressure transients in-air for blast of a 1.5-mm thick PET burst membrane. The peak overpressure [denoted by point (C)] for this blast was 534 kPa with a duration of 1.040 ms and an impulse of 184 kPa-ms. (B) The output of the shock tube was similar in shape to the Friedlander wave, which models the primary blast produced from an explosion in the free-field. (C) For the open shock tube, the durations were plotted as a function of the peak overpressures for each blast and fit to a second-order polynomial (n = 78). (D) For the open tube, the impulses were plotted as a function of peak overpressures for each blast and fit to a second-order polynomial (n = 78).
Mentions: Characterization of the shock tube was performed without the receiver in place (Figure 2). Pressure time-histories recorded at the end of the shock tube were typical of a Friedlander wave (Figure 2B) and demonstrated good inter-test consistency (Figure 2A). Duration of the positive pressure phase was correlated with peak overpressure, and the relationship was well-defined by a second-order polynomial fit (Figure 2C). The impulse was also correlated with peak overpressure and was well-defined by a second-order polynomial as well (Figure 2D).

Bottom Line: Blast-induced traumatic brain injury (bTBI) results from the translation of a shock wave in-air, such as that produced by an IED, into a pressure wave within the skull-brain complex.To better prevent and treat bTBI, both the initiating biomechanics and the ensuing pathobiology must be understood in greater detail.A well-characterized, in vitro model of bTBI, in conjunction with animal models, will be a powerful tool for developing strategies to mitigate the risks of bTBI.

View Article: PubMed Central - PubMed

Affiliation: Department of Biomedical Engineering, Columbia University New York, NY, USA.

ABSTRACT
Due to the prominent role of improvised explosive devices (IEDs) in wounding patterns of U.S. war-fighters in Iraq and Afghanistan, blast injury has risen to a new level of importance and is recognized to be a major cause of injuries to the brain. However, an injury risk-function for microscopic, macroscopic, behavioral, and neurological deficits has yet to be defined. While operational blast injuries can be very complex and thus difficult to analyze, a simplified blast injury model would facilitate studies correlating biological outcomes with blast biomechanics to define tolerance criteria. Blast-induced traumatic brain injury (bTBI) results from the translation of a shock wave in-air, such as that produced by an IED, into a pressure wave within the skull-brain complex. Our blast injury methodology recapitulates this phenomenon in vitro, allowing for control of the injury biomechanics via a compressed-gas shock tube used in conjunction with a custom-designed, fluid-filled receiver that contains the living culture. The receiver converts the air shock wave into a fast-rising pressure transient with minimal reflections, mimicking the intracranial pressure history in blast. We have developed an organotypic hippocampal slice culture model that exhibits cell death when exposed to a 530 ± 17.7-kPa peak overpressure with a 1.026 ± 0.017-ms duration and 190 ± 10.7 kPa-ms impulse in-air. We have also injured a simplified in vitro model of the blood-brain barrier, which exhibits disrupted integrity immediately following exposure to 581 ± 10.0 kPa peak overpressure with a 1.067 ± 0.006-ms duration and 222 ± 6.9 kPa-ms impulse in-air. To better prevent and treat bTBI, both the initiating biomechanics and the ensuing pathobiology must be understood in greater detail. A well-characterized, in vitro model of bTBI, in conjunction with animal models, will be a powerful tool for developing strategies to mitigate the risks of bTBI.

No MeSH data available.


Related in: MedlinePlus