Abstract
Explosive blast results in multiple organ injury and polytrauma, the intensity of which varies with the nature of the exposure, orientation, environment and individual resilience. Blast overpressure alone may not precisely indicate the level of body or brain injury after blast exposure. Assessment of the extent of body injury after blast exposure is important, since polytrauma and systemic factors significantly contribute to blast-induced traumatic brain injury. We evaluated the activity of plasma enzymes including aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH) and creatine kinase (CK) at different time points after blast exposure using a mouse model of single and repeated blast exposures to assess the severity of injury. Our data show that activities of all the enzymes in the plasma were significantly increased as early as 1 h after blast exposure. The elevated enzyme activity remained up to 6 h in an overpressure dose-dependent manner and returned close to normal levels at 24 h. Head-only blast exposure with body protection showed no increase in the enzyme activities suggesting that brain injury alone does not contribute to the systemic increase. In contrast to plasma increase, AST, ALT and LDH activity in the liver and CK in the skeletal muscle showed drastic decrease at 6 h after blast exposures. Histopathology showed mild necrosis at 6 h and severe necrosis at 24 h after blast exposures in liver and no changes in the skeletal muscle suggesting that the enzyme release from the tissue to plasma is probably triggered by transient cell membrane disruption from shockwave and not due to necrosis. Overpressure dependent transient release of tissue enzymes and elevation in the plasma after blast exposure suggest that elevated enzyme activities in the blood can be potentially used as a biological dosimeter to assess the severity of blast injury.
Highlights
The frequency of blast-induced traumatic brain injury has been increased tremendously in the recent conflicts due to the high use of improvised explosive devises [1,2]
Torso protection but not head protection significantly attenuated blast neurotrauma indicating that blast mediated organ injury, polytrauma and systemic response plays a vital role in the development of primary blast neurotrauma [13,14]
Using an in vitro blast TBI model system with shock tube, we have shown that blast exposure leads to the release of lactate dehydrogenase (LDH) from the cells to the culture medium without cell mortality and suggested that blast-induced plasma membrane damage as a potential mechanism of this enzyme release [36]
Summary
The frequency of blast-induced traumatic brain injury (blast TBI) has been increased tremendously in the recent conflicts due to the high use of improvised explosive devises [1,2]. The neuropathology and subsequent cognitive deficits after blast exposure are proposed to be a cumulative effect of direct blast overpressure effect on the brain along with damage to other body organs [9,10,11]. Protective Kevlar body vests decreased the mortality, neuropathology and behavioral deficits in rats exposed to blast overpressure supporting the notion that polytrauma and systemic effects significantly contribute to blast TBI [12]. It has been reported that blast exposure to torso after head protection produce more severe neurotrauma compared to headonly exposure supporting that body injury, polytrauma and systemic factors play a significant role in blast TBI [13,14]. Systemic response along with transient torso to brain hydraulic overpressure transmission leads to blood-brain barrier breakdown, neuroinflammation, cerebral vasospasm and blast neurotrauma [3,13,15,16,17,18,19,20,21]
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