title: Effect of albumin and Hespan on rodent hepatocyte function after hemorrhagic shock and sepsis.
abstract: BACKGROUND
  Sepsis and hemorrhagic shock (HS) cause hypoalbuminemia, with extravascular albumin relocation. Prior studies on cultured rat hepatocytes showed a fall in albumin genesis when exposed to albumin and Hespan (HES) supplementation. This study assesses the effects of increased colloid osmotic pressure on albumin and urea genesis from hepatocytes exposed to HS or septic insult before harvesting.
  
  
  METHODS
  Hepatocyte synthesis of albumin was measured in an in vitro collagen sandwich preparation with a seeding density of 1 million cells per dish in Dulbecco's modified Eagle's medium without additional colloid (control cultures). Study groups included control plus 2% bovine serum albumin (BSA), 4% BSA, 2% HES, and 4% HES.
  
  
  RESULTS
  The albumin secretion in the control cultures of HS cells rose from 19.03 microg/d/10(6) cells on day 3 to 88.81 microg/d/10(6) cells by day 8 and remained constant. In contrast, albumin genesis in the 2% and 4% BSA groups rose from a significantly higher (p < 0.05) day 3 value of 39.83 microg/d/10(6) cells and 48.76 microg/d/10(6) cells, respectively, to 116.39 microg/d/10(6) cells and 118.76 microg/d/10(6) cells by day 8 and remained fairly constant. Albumin genesis from the HS cells after 2% HES and 4% HES was similar to control HS cells through day 8 but was significantly greater by day 12. Urea genesis from HS cells was greater in the 4% HES group compared with control and the 2% BSA and 4% BSA groups. The albumin genesis in the control cultures of septic cells was 9.32 microg/d/10(6) cells on day 3, rose to 81.46 microg/d/10(6) cells by day 8, and remained fairly constant. The BSA-supplemented septic cells had significantly higher albumin output than control cells early in the experiment, whereas the 2% HES group had higher albumin secretion than control cells throughout the study.
  
  
  CONCLUSIONS
  HS and septic cultured hepatocytes respond to a rise in interstitial colloid osmotic pressure with a rise in albumin genesis, associated with morphologic changes typical of cellular injury. The mechanism remains cryptic; studies on human hepatocytes are needed.
authors.affiliation: Department of Surgery, Wayne State University, Detroit, Michigan, USA.
authors.forename: Angie L
authors.initials: AL
authors.lastname: Vlahos
authors.forename: Robert S
authors.initials: RS
authors.lastname: Crawford
authors.forename: Howard T
authors.initials: HT
authors.lastname: Matthew
authors.forename: Anna M
authors.initials: AM
authors.lastname: Ledgerwood
authors.forename: Charles E
authors.initials: CE
authors.lastname: Lucas
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D002478:Cells, Cultured; D022781:Hepatocytes / Q000378:metabolism*; D006895:Hydroxyethyl Starch Derivatives / Q000627:therapeutic use*; D007019:Hypoproteinemia / Q000517:prevention & control; D008297:Male; D009997:Osmotic Pressure; D010952:Plasma Substitutes / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012709:Serum Albumin / Q000096:biosynthesis / Q000627:therapeutic use*; D012771:Shock, Hemorrhagic / Q000473:pathology / Q000628:therapy*; D012772:Shock, Septic / Q000473:pathology / Q000628:therapy*; D014508:Urea / Q000378:metabolism
chemical_list: D006895:Hydroxyethyl Starch Derivatives; D010952:Plasma Substitutes; D012709:Serum Albumin; D014508:Urea