• R Härtl, M B Medary, M Ruge, K E Arfors, F Ghahremani, and J Ghajar.
• Aitken Neuroscience Institute, New York, NY 10021, USA.
• J Trauma. 1997 May 1;42(5 Suppl):S41-7.

BackgroundTraumatic 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.MethodsRabbits 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).ResultsTBI 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.ConclusionsWhether 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.

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