title: Fluid resuscitation with isotonic or hypertonic saline solution avoids intraneural calcium influx after traumatic brain injury associated with hemorrhagic shock.
abstract: BACKGROUND
  Calcium is one of the triggers involved in ischemic neuronal death. Because hypotension is a strong predictor of outcome in traumatic brain injury (TBI), we tested the hypothesis that early fluid resuscitation blunts calcium influx in hemorrhagic shock associated to TBI.
  
  
  METHODS
  Fifteen ketamine-halothane anesthetized mongrel dogs (18.7 kg +/- 1.4 kg) underwent unilateral cryogenic brain injury. Blood was shed in 5 minutes to a target mean arterial pressure of 40 mm Hg to 45 mm Hg and maintained at these levels for 20 minutes (shed blood volume = 26 mL/kg +/- 7 mL/kg). Animals were then randomized into three groups: CT (controls, no fluid resuscitation), HS (7.5% NaCl, 4 mL/kg, in 5 minutes), and LR (lactate Ringer's, 33 mL/kg, in 15 minutes). Twenty minutes later, a craniotomy was performed and cerebral biopsies were obtained next to the lesion ("clinical penumbra") and from the corresponding contralateral side ("lesion's mirror") to determine intracellular calcium by fluorescence signals of Fura-2-loaded cells.
  
  
  RESULTS
  Controls remained hypotensive and in a low-flow state, whereas fluid resuscitation improved hemodynamic profile. There was a significant increase in intracellular calcium in the injured hemisphere in CT (1035 nM +/- 782 nM), compared with both HS (457 nM +/- 149 nM, p = 0.028) and LR (392 nM +/- 178 nM, p = 0.017), with no differences between HS and LR (p = 0.38). Intracellular calcium at the contralateral, uninjured hemisphere was 438 nM +/- 192 nM in CT, 510 nM +/- 196 nM in HS, and 311 nM +/- 51 nM in LR, with no significant differences between them.
  
  
  CONCLUSIONS
  Both small volume hypertonic saline and large volume lactated Ringer's blunts calcium influx in early stages of TBI associated to hemorrhagic shock. No fluid resuscitation strategy promotes calcium influx and further neural damage.
authors.affiliation: Department of Surgery, Federal University of São Paulo, São Paulo, Brazil.
authors.forename: Marcos
authors.initials: M
authors.lastname: Balbino
authors.forename: Antonio
authors.initials: A
authors.lastname: Capone Neto
authors.forename: Ricardo
authors.initials: R
authors.lastname: Prist
authors.forename: Alice Teixeira
authors.initials: AT
authors.lastname: Ferreira
authors.forename: Luiz F
authors.initials: LF
authors.lastname: Poli-de-Figueiredo
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001706:Biopsy; D001930:Brain Injuries / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism* / Q000503:physiopathology; D002118:Calcium / Q000378:metabolism*; D002302:Cardiac Output / Q000502:physiology; D002560:Cerebrovascular Circulation / Q000187:drug effects; D003399:Craniotomy; D004285:Dogs; D005440:Fluid Therapy / Q000379:methods*; D006439:Hemodynamics / Q000187:drug effects; D007427:Intracranial Pressure / Q000187:drug effects; D007552:Isotonic Solutions / Q000494:pharmacology*; D008297:Male; D008991:Monitoring, Physiologic; D011897:Random Allocation; D012462:Saline Solution, Hypertonic / Q000494:pharmacology*; D012771:Shock, Hemorrhagic / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism* / Q000503:physiopathology; D018709:Statistics, Nonparametric; D013990:Tidal Volume / Q000502:physiology
chemical_list: D007552:Isotonic Solutions; D012462:Saline Solution, Hypertonic; D002118:Calcium