title: The effect of hypertonic saline resuscitation on responses to severe hemorrhagic shock by the skeletal muscle, intestinal, and renal microcirculation systems: seeing is believing.
abstract: BACKGROUND
  Decompensated hemorrhagic shock is often refractory to resuscitation, and we show here that it is associated with loss of vascular tone in skeletal muscle precapillary arterioles. We tested the hypothesis that microvascular derangements in the skeletal muscle, intestinal, and renal microcirculation systems would be reversed by initial hypertonic saline-dextran infusion.
  
  
  METHODS
  Male Sprague-Dawley rats underwent precollicular brain stem transection without anesthesia for study. Parameters measured by in vivo videomicroscopy included cardiac output, mean arterial pressure, and microvascular responses in the skeletal muscle, ileum, and renal (i.e., the hydronephrotic kidney) microcirculation systems. Hemorrhaged was induced to a mean arterial pressure of 50 mmHg until decompensation occurred. The rats were then initially resuscitated with (1) 4 mL/kg 7.5% NaCl in 6% dextran 70, (2) 33 mL/kg .9% NaCl in 6% dextran 70, or (3) 33 mL/kg .9% NaCl. Twenty minutes later they received shed blood plus 33 mL/kg .9% NaCl to maintain mean arterial pressure at baseline levels.
  
  
  RESULTS
  Decompensated hemorrhagic shock decreased cardiac output to between 24% and 35% of baseline values and profoundly decreased microvascular blood flow to between 10% and 19% of baseline. At the completion of resuscitation cardiac output increased to greater than baseline in all groups. Microvascular blood flow increased toward baseline transiently but then progressively deteriorated to between 36% and 69% of baseline in the 3 tissues. There was no significant difference between the three resuscitative fluids.
  
  
  CONCLUSIONS
  Despite return of cardiac output to greater than baseline levels, muscle, intestinal, and renal microvascular blood flows remained significantly depressed. Hypertonic saline and/or dextran did not improve these deficits.
authors: Department of Surgery, University of California Los Angeles Medical Center, 10833 Le Conte Ave., 72-178 CHS, Los Angeles, CA 90095, USA. hcryer@mednet.ucla.edu
authors: Henry M
authors: HM
authors: Cryer
authors: John
authors: J
authors: Gosche
authors: Jeff
authors: J
authors: Harbrecht
authors: Greg
authors: G
authors: Anigian
authors: Neal
authors: N
authors: Garrison
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D004195:Disease Models, Animal; D006439:Hemodynamics / Q000502:physiology*; D007421:Intestine, Small / Q000098:blood supply; D007668:Kidney / Q000098:blood supply*; D008297:Male; D008833:Microcirculation / Q000502:physiology; D018482:Muscle, Skeletal / Q000098:blood supply*; D011336:Probability; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012151:Resuscitation / Q000379:methods*; D012307:Risk Factors; D012462:Saline Solution, Hypertonic / Q000494:pharmacology*; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D012771:Shock, Hemorrhagic / Q000401:mortality / Q000628:therapy*; D015996:Survival Rate
chemical_list: D012462:Saline Solution, Hypertonic