Secondary hypoxia following moderate fluid percussion brain injury in rats exacerbates sensorimotor and cognitive deficits.

Human head trauma is frequently associated with respiratory problems resulting in secondary hypoxic insult. To document the behavioral consequences of secondary hypoxia in an established model of traumatic brain injury (TBI), intubated anesthetized animals were subjected to fluid percussion (FP) injury (1.87-2.17 atm) followed by 30 min of either normoxic (TBI-NO, n = 10) or hypoxic (TBI-HY, n = 11; pO2 = 30-40 mm Hg) gas levels. Sham animals (n = 19) underwent all manipulations except for the actual trauma. Animals were tested on various sensorimotor tasks beginning 3 days after FP injury along with cognitive testing on days 22 through 29 posttrauma. The secondary hypoxic insult exacerbated the sensorimotor deficits on beam-walking compared to those animals only receiving trauma. Cognitive impairments were also observed in the TBI-HY group in the hidden platform task compared to FP injury alone. These data indicate that a secondary hypoxic insult exacerbates both sensorimotor and cognitive deficits after TBI. This study provides direct evidence that incidences of hypoxia after brain trauma may potentially result in an increase in neurological deficits for the subpopulation of head injured patients undergoing hypoxic conditions further warranting strict monitoring of these events.