title: Hemorrhagic shock and resuscitation-mediated tissue water distribution is normalized by adjunctive peritoneal resuscitation.
abstract: BACKGROUND
  Adjunctive direct peritoneal resuscitation (DPR) from hemorrhagic shock (HS) improves intestinal blood flow and abrogates postresuscitation edema. HS causes water shifts as a result of sodium redistribution and changes in transcapillary Starling forces. Conventional resuscitation (CR) with crystalloid aggravates water sequestration. We examined the compartment pattern of organ tissue water after HS and CR, and modulation of tissue edema by adjunctive DPR.
  
  
  METHODS
  Rats were hemorrhaged (40% mean arterial pressure for 60 minutes) and assigned to four groups (n = 7): sham, no HS; HS no resuscitation; HS+CR (shed blood plus 2 volumes Ringer's lactate); and HS+CR+DPR (20 mL clinical intraperitoneal (IP) dialysis fluid). Isotopic markers determined equilibrium distribution volumes [V(D)] in gut, liver, lung, and muscle by quantitative autoradiography (2-hour postresuscitation). Total tissue water (TTW) was determined by wet-dry weights. Extracellular water was measured from (14)C-mannitol V(D), and intravascular volume (IVV) from (131)I-labeled IgG V(D). Cellular and interstitial water volumes were calculated.
  
  
  RESULTS
  HS alone decreased IVV in all tissues and TTW in gut, lung, and muscle, but not liver, compared with shams. IVV remained decreased with all resuscitations despite restoration of central hemodynamics. CR caused interstitial edema in gut, liver, and muscle, and cellular edema in lung. DPR reduced (liver, muscle) or prevented (gut, lung) these volume shifts.
  
  
  CONCLUSIONS
  HS decreases IVV. HS-induced water shifts are organ-specific and prominent in gut, lung, and muscle. CR restores central hemodynamics, does not restore IVV, and alters organ-specific TTW distribution. Adjunctive DPR with IP dialysis fluid normalizes TTW and water compartment distribution and prevents edema. Combined effect of DPR and intravascular fluid replacement appears to prevent global tissue edema and improve outcomes from HS.
authors.affiliation: Department of Physiology and Biophysics, University of Louisville, Louisville, KY 40292, USA. erzaka01@louisville.edu
authors.forename: El Rasheid
authors.initials: el R
authors.lastname: Zakaria
authors.forename: Paul J
authors.initials: PJ
authors.lastname: Matheson
authors.forename: Michael F
authors.initials: MF
authors.lastname: Flessner
authors.forename: R Neal
authors.initials: RN
authors.lastname: Garrison
mesh_terms: D000818:Animals; D001803:Blood Transfusion; D004195:Disease Models, Animal; D004487:Edema / Q000209:etiology / Q000503:physiopathology*; D005440:Fluid Therapy; D008297:Male; D010530:Peritoneal Dialysis / Q000379:methods*; D010537:Peritoneum; D051381:Rats; D017207:Rats, Sprague-Dawley; D012151:Resuscitation / Q000379:methods*; D012771:Shock, Hemorrhagic / Q000150:complications / Q000503:physiopathology / Q000628:therapy*; D014882:Water-Electrolyte Balance / Q000502:physiology; D014883:Water-Electrolyte Imbalance / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*