No abstract

Exposure to blast overpressure (BOP) activates a cascade of pathological processes including changes in intracranial pressure (ICP) and blood-brain barrier (BBB) permeability resulting in traumatic brain injury (TBI). In this study the effect of single and multiple exposures at two intensities of BOP on changes in ICP and BBB permeability in Sprague-Dawley rats was evaluated. Animals were exposed to a single or three repetitive (separated by 0.5 h) BOPs at 72 kPa or 110 kPa. ICP was monitored continuously via telemetry for 6 days after exposure to BOP. The alteration in the permeability of BBB was determined by extravasation of Evans Blue (EB) into brain parenchyma. A significant increase in ICP was observed in all groups except the single 72 kPa BOP group. At the same time a marked increase in BBB permeability was also seen in various parts of the brain. The extent of ICP increase as well as BBB permeability change was dependent on intensity and frequency of blast.

Objective: Intermittency is routinely used as a protective strategy against CNS and pulmonary hyperbaric oxygen (HBO2) toxicity, however exact mechanisms of protection are not known. This study was designed to optimize intermittent HBO2 exposures by variable duration of HBO2 cycles. Methods: Rats were exposed to O2 at 2.8 ATA delivered either continuously for 6 h or intermittently with 10 min air breaks. Two intermittent paradigms were used; the first consisted of longer HBO2 60 min cycles at the beginning and shorter 30 min cycles at the end of exposure, while in the second paradigm, shorter cycles were followed by longer HBO2 cycles. Effectiveness of intermittency was assessed by gene expression of inflammatory cytokines TNF-α, IL-1β, IL-6 and heat shock protein 70 (HSP70) in the lungs at the end of exposures. The gene expression was compared with changes in respiration detected by continuous recording of respiration by a modified version of the whole-body plethysmography. Results: All intermittent schedules inhibited lung inflammation compared with the continuous exposures. Efficacy of this inhibition was significantly better in intermittent groups starting with longer duration of HBO2 cycles than in groups with reversed duration of HBO2 cycles. Intermittent exposures starting with longer HBO2 cycles also slowed down changes in respiratory frequency and tidal volume compared with the continuous exposure. HSP70 was increased in all exposure groups. It was significantly higher in continuous exposures and in intermittent group starting with longer duration of HBO2 cycles than in the group starting with shorter HBO2 cycles. Conclusions: The higher benefit of the initially longer HBO2 cycles could be in part explained by a higher oxidative stress and higher HSP70 expression in lungs compared with exposures with initially shorter HBO2 cycles. [J Exp Integr Med 2012; 2(4): 287-296