Abstract
To determine the effects of mild blast-induced traumatic brain injury (bTBI), several groups of rats were subjected to blast injury or sham injury in a compressed air-driven shock tube. The effects of bTBI on relative cerebral perfusion (laser Doppler flowmetry [LDF]), and mean arterial blood pressure (MAP) cerebral vascular resistance were measured for 2 h post-bTBI. Dilator responses to reduced intravascular pressure were measured in isolated middle cerebral arterial (MCA) segments, ex vivo, 30 and 60 min post-bTBI. Neuronal injury was assessed (Fluoro-Jade C [FJC]) 24 and 48 h post-bTBI. Neurological outcomes (beam balance and walking tests) and working memory (Morris water maze [MWM]) were assessed 2 weeks post-bTBI. Because impact TBI (i.e., non-blast TBI) is often associated with reduced cerebral perfusion and impaired cerebrovascular function in part because of the generation of reactive oxygen and nitrogen species such as peroxynitrite (ONOO−), the effects of the administration of the ONOO− scavenger, penicillamine methyl ester (PenME), on cerebral perfusion and cerebral vascular resistance were measured for 2 h post-bTBI. Mild bTBI resulted in reduced relative cerebral perfusion and MCA dilator responses to reduced intravascular pressure, increases in cerebral vascular resistance and in the numbers of FJC-positive cells in the brain, and significantly impaired working memory. PenME administration resulted in significant reductions in cerebral vascular resistance and a trend toward increased cerebral perfusion, suggesting that ONOO− may contribute to blast-induced cerebral vascular dysfunction.
Highlights
Traumatic brain injury (TBI) is one of the most common types of injuries among combatants in Operations Iraqi Freedom, Enduring Freedom, and New Dawn[1,2,3,4,5] in part because of the high incidence of blast-induced TBI
Dilator responses to progressive reductions in intravascular pressure were significantly reduced in the 30 min ( p = 0.01, blast-induced TBI (bTBI) vs. sham) and 60 min ( p = 0.02, bTBI vs. sham) Advanced Blast Simulator (ABS) bTBI groups after blast exposure (Fig. 3)
Our results indicated that mild bTBI was associated with significant reductions in relative cerebral perfusion and increases in cerebral vascular resistance that occurred within 5 min and persisted for at least 2 h post-bTBI
Summary
Traumatic brain injury (TBI) is one of the most common types of injuries among combatants in Operations Iraqi Freedom, Enduring Freedom, and New Dawn[1,2,3,4,5] in part because of the high incidence of blast-induced TBI (bTBI). TBI was followed by cerebral hypoperfusion in some patients[18,19,20] and in experimental animals.[21,22,23] Clinical TBI24 and fluid-percussion injury[25,26,27] were associated with impaired cerebral vascular responses to changes in arterial blood pressure (i.e., pressure autoregulation).[24,25,26,27] Impact TBI was associated with impaired cerebral vascular compensatory responses to changes in the partial pressures of carbon dioxide,[28,29,30] oxygen,[31] and hematocrit.[32] Like impact TBI, bTBI resulted in some degree of cerebral vascular injury with recent evidence of level-dependent reductions in relative blood flow in the cortex and hippocampus of rats exposed to several shock-wave intensities in an air-driven shock tube.[33] Both
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