title: Hypertonic saline resuscitation of hemorrhagic shock does not decrease in vivo neutrophil interactions with endothelium in the blood-brain microcirculation.
abstract: BACKGROUND
  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 with endothelial cells (EC) in systemic microvascular beds, no data exist demonstrating that the same occurs in the unique blood-brain barrier microcirculation. We hypothesized that resuscitation of hemorrhagic shock with HTS would blunt brain in vivo PMN-EC interactions.
  
  
  METHODS
  Wistar rats (250-350 g) underwent craniotomy and placement of a window for live intravital viewing of pial vessels. Twenty animals were bled to a mean arterial pressure of 30 mm Hg to 35 mm Hg for 1 hour and resuscitated with shed blood and either 5% HTS (6 mL/kg) or Ringer's lactate (RL) (2× shed blood volume). Circulating rhodamine-6G-labeled PMN in pial venules were captured by videomicroscopy at baseline (preshock), end of the shock period, after resuscitation, and every 15 minutes to 30 minutes for 2 hours. Hemodynamics and arterial gases were monitored. Off-line footage analysis allowed comparisons of PMN-EC interactions between groups.
  
  
  RESULTS
  Animals in both groups developed significant metabolic acidosis (p < 0.01) after hemorrhage, but postresuscitation blood pressures were similar at all time points. Crystalloid resuscitation volumes were 10× greater in RL than HTS animals (p < 0.001). For all time points, we did not observe the expected reduction in PMN rolling and adhesion in HTS animals, instead noted trends of consistently lower interactions in RL counterparts.
  
  
  CONCLUSIONS
  In contradistinction to studies evaluating the systemic microcirculation, HTS may activate PMN-EC crosstalk in the blood-brain microcirculation. Further studies are needed to analyze whether this effect is due to the unique nature of the blood-brain interface.
authors.affiliation: Division of Traumatology, Surgical Critical Care & Emergency Surgery, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.
authors.forename: Wanfeng
authors.initials: W
authors.lastname: Gong
authors.forename: Joshua A
authors.initials: JA
authors.lastname: Marks
authors.forename: Paymon
authors.initials: P
authors.lastname: Sanati
authors.forename: Carrie
authors.initials: C
authors.lastname: Sims
authors.forename: Babak
authors.initials: B
authors.lastname: Sarani
authors.forename: Douglas H
authors.initials: DH
authors.lastname: Smith
authors.forename: Jose L
authors.initials: JL
authors.lastname: Pascual
mesh_terms: D000818:Animals; D001812:Blood-Brain Barrier / Q000502:physiology*; D004195:Disease Models, Animal; D042783:Endothelial Cells / Q000502:physiology*; D004730:Endothelium, Vascular / Q000166:cytology / Q000502:physiology*; D007552:Isotonic Solutions; D008297:Male; D008833:Microcirculation / Q000502:physiology; D009504:Neutrophils / Q000502:physiology*; D051381:Rats; D000077325:Ringer's Lactate; D012462:Saline Solution, Hypertonic / Q000627:therapeutic use*; D012771:Shock, Hemorrhagic / Q000628:therapy*
chemical_list: D007552:Isotonic Solutions; D000077325:Ringer's Lactate; D012462:Saline Solution, Hypertonic