Hypertonic Saline Resuscitation of Hemorrhagic Shock Does Not Decrease In Vivo Neutrophil Interactions With Endothelium in the Blood-Brain Microcirculation

Hypertonic saline Intravital microscopy
DOI: 10.1097/ta.0b013e318226eb51 Publication Date: 2011-08-09T08:56:33Z
ABSTRACT
Resuscitation of hemorrhagic shock with isotonic crystalloids has been shown to activate polymorphonuclear neutrophils (PMNs). Although hypertonic saline (HTS) can reduce PMN activation and interactions endothelial cells (EC) in systemic microvascular beds, no data exist demonstrating that the same occurs unique blood-brain barrier microcirculation. We hypothesized resuscitation HTS would blunt brain vivo PMN-EC interactions.Wistar rats (250-350 g) underwent craniotomy placement a window for live intravital viewing pial vessels. Twenty animals were bled mean arterial pressure 30 mm Hg 35 1 hour resuscitated shed blood either 5% (6 mL/kg) or Ringer's lactate (RL) (2× volume). Circulating rhodamine-6G-labeled venules captured by videomicroscopy at baseline (preshock), end period, after resuscitation, every 15 minutes 2 hours. Hemodynamics gases monitored. Off-line footage analysis allowed comparisons between groups.Animals both groups developed significant metabolic acidosis (p < 0.01) hemorrhage, but postresuscitation pressures similar all time points. Crystalloid volumes 10× greater RL than 0.001). For points, we did not observe expected reduction rolling adhesion animals, instead noted trends consistently lower counterparts.In contradistinction studies evaluating microcirculation, may crosstalk Further are needed analyze whether this effect is due nature interface.
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