ABSTRACT
BACKGROUND: Traumatic brain injury (TBI) induces an acute inflammatory response characterized by early recruitment of inflammatory cells (white blood cells). Rapid resuscitation of TBI with hypertonic saline/dextran (HS/DEX) yields promising results in clinical and experimental studies. The purpose of this paper was to test the hypothesis that HS/DEX exerts its effects in part through a modulation of the acute inflammatory response to TBI. METHODS: Rabbits equipped with chronic cranial windows underwent fluid-percussion injury and were followed up for 6 hours. Intravital fluorescence videomicroscopy technique was used to visualize white blood cell trafficking and to measure pia vessel diameters and venular shear rates. Three groups were studied: sham (group I, n = 5), trauma (group II, n = 7), and trauma and 4 mL/kg 7.2% NaCl/10% dextran 60 IV over 5 minutes at 10 minutes after TBI (group III, n = 7). RESULTS: TBI in groups II and III led to significant increases of intracranial pressure. Arteriolar diameters after trauma increased by 17 +/- 8% at 6 hours in group II. Infusion of HS/DEX completely prevented this secondary diameters increase. At 6 hours, the increase of "sticking" white blood cells in group III was reduced by approximately 90% compared with group II. CONCLUSIONS: Whether the anti-inflammatory effect of HS/DEX plays a role in reducing delayed brain damage (> 6 hours after TBI) or other systemic complications of TBI arises as an important question and should be investigated further.
