title: Fluid resuscitation does not improve renal oxygenation during hemorrhagic shock in rats.
abstract: BACKGROUND
  The resuscitation strategy for hemorrhagic shock remains controversial, with the kidney being especially prone to hypoxia.
  
  
  METHODS
  The authors used a three-phase hemorrhagic shock model to investigate the effects of fluid resuscitation on renal oxygenation. After a 1-h shock phase, rats were randomized into four groups to receive either normal saline or hypertonic saline targeting a mean arterial pressure (MAP) of either 40 or 80 mmHg. After such resuscitation, rats were transfused with the shed blood. Renal macro- and microcirculation were monitored with cortical and outer-medullary microvascular oxygen pressure, renal oxygen delivery, and renal oxygen consumption measured using oxygen-dependent quenching of phosphorescence.
  
  
  RESULTS
  Hemorrhagic shock was characterized by a drop of aortic blood flow, MAP, renal blood flow, renal oxygen delivery, renal oxygen consumption, and renal microvascular PO2. During the fluid resuscitation phase, normal saline targeting a MAP = 80 mmHg was the sole strategy able to restore aortic blood flow, renal blood flow, and renal oxygen consumption, although without improving renal oxygen delivery. However, none of the strategies using either normal saline or hypertonic saline or targeting a high MAP could restore the renal microvascular Po2. Blood transfusion increased microvascular Po2 but was unable to totally restore renal microvascular oxygenation to baseline values.
  
  
  CONCLUSIONS
  This experimental rat study shows that (1) high MAP-directed fluid resuscitation (80 mmHg) does not lead to higher renal microvascular Po2 compared with fluid resuscitation targeted to MAP (40 mmHg); (2) hypertonic saline is not superior to normal saline regarding renal oxygenation; and (3) decreased renal oxygenation persists after blood transfusion.
authors.affiliation: Department of Translational Physiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. m.legrand@libertysurf.fr
authors.forename: Matthieu
authors.initials: M
authors.lastname: Legrand
authors.forename: Egbert G
authors.initials: EG
authors.lastname: Mik
authors.forename: Gianmarco M
authors.initials: GM
authors.lastname: Balestra
authors.forename: Rene
authors.initials: R
authors.lastname: Lutter
authors.forename: Romain
authors.initials: R
authors.lastname: Pirracchio
authors.forename: Didier
authors.initials: D
authors.lastname: Payen
authors.forename: Can
authors.initials: C
authors.lastname: Ince
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001803:Blood Transfusion; D005440:Fluid Therapy; D006439:Hemodynamics / Q000502:physiology; D007249:Inflammation / Q000473:pathology; D007668:Kidney / Q000378:metabolism*; D007677:Kidney Function Tests; D019344:Lactic Acid / Q000097:blood; D008297:Male; D008833:Microcirculation / Q000502:physiology; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012079:Renal Circulation / Q000502:physiology; D012151:Resuscitation; D012462:Saline Solution, Hypertonic; D012771:Shock, Hemorrhagic / Q000378:metabolism*; D014882:Water-Electrolyte Balance / Q000502:physiology
chemical_list: D012462:Saline Solution, Hypertonic; D019344:Lactic Acid; D010100:Oxygen