title: Correlation between red blood cell deformability and changes in hemodynamic function.
abstract: BACKGROUND
  In sepsis red blood cells (RBCs) have been shown to be less deformable (i.e., more rigid) and have been implicated in decreasing nutrient blood supply and possibly leading to organ dysfunction. However, no studies have demonstrated an association between organ dysfunction and rigid RBCs. This study examined cardiovascular physiologic and histologic changes in two different models to determine whether a relationship may exist between RBC deformability and organ function.
  
  
  METHODS
  In the following two experiments, cardiac index (CI) was continuously measured, whereas both deformability index and histology were examined at the end of the experimental periods. The first experiment studied nonanesthetized, hydrated rats after a cecal ligation and puncture (CLP), a slow-developing means of inducing RBC rigidity. In a second experiment animals were anesthetized and received a 20% total blood volume transfusion of either diamide-treated (rigid) RBCs or normal RBCs.
  
  
  RESULTS
  CLP-treated animals' CI gradually decreased during 18 hours (232 +/- 60 ml/min/kg to 123 +/- 90 ml/min/kg; p = 0.05), with an increase in systemic vascular resistance (1459 +/- 517 dyne.sec/cm5.m2 to 2337 +/- 1213 dyne.sec/cm5.m2; p = 0.02). Diamide-treated animals had a rapid decrease in CI (86 +/- 7.0 ml/min/kg to 58 +/- 13 ml/min/kg; p = 0.05) and increase in SVR (2269 +/- 373 dyne.sec/cm5.m2 to 3897 +/- 988 dyne.sec/cm5.m2; p = 0.05) from baseline to 120 minutes after treatment respectively. The DI was significantly lower in both CLP and diamide groups (p < 0.03) when compared with control animals. Histologic evidence of subendocardial necrosis was shown in both the CLP- and Diamide-treated animals.
  
  
  CONCLUSIONS
  These data suggest an association with RBC deformability and organ function in both septic and nonseptic animal models.
authors.affiliation: Department of Surgery, UMD-New Jersey Medical School, Newark 07103.
authors.forename: J E
authors.initials: JE
authors.lastname: Langenfeld
authors.forename: G W
authors.initials: GW
authors.lastname: Machiedo
authors.forename: M
authors.initials: M
authors.lastname: Lyons
authors.forename: B F
authors.initials: BF
authors.lastname: Rush
authors.forename: G
authors.initials: G
authors.lastname: Dikdan
authors.forename: T W
authors.initials: TW
authors.lastname: Lysz
mesh_terms: D000818:Animals; D002432:Cecum; D003958:Diamide / Q000494:pharmacology; D004699:Endocardium / Q000473:pathology; D004907:Erythrocyte Deformability / Q000187:drug effects; D004912:Erythrocytes / Q000187:drug effects / Q000378:metabolism; D006439:Hemodynamics / Q000502:physiology*; D008026:Ligation; D008168:Lung / Q000473:pathology; D008297:Male; D009336:Necrosis; D010100:Oxygen / Q000097:blood; D011677:Punctures; D051381:Rats; D017207:Rats, Sprague-Dawley; D018805:Sepsis / Q000097:blood*; D014810:Vitamin E / Q000494:pharmacology
chemical_list: D003958:Diamide; D014810:Vitamin E; D010100:Oxygen