title: Pulmonary and extrapulmonary effects of increased colloid osmotic pressure during endotoxemia in rats.
abstract: OBJECTIVE
  We tested the hypothesis that an increase in the blood colloid osmotic pressure (COP) that is maintained during early-stage endotoxemia may decrease fluid flux across capillaries and may reduce pulmonary and multiple-organ edema.
  
  
  METHODS
  Prospective study.
  
  
  METHODS
  Research laboratory in a hospital.
  
  
  METHODS
  Male albino Sprague-Dawley rats.
  
  
  METHODS
  Rats were anesthetized with pentobarbital, underwent tracheotomies, were cannulated in the femoral vein and artery, and were randomly assigned to the following four groups comprising 11 rats each: group I, controls (saline solution treatment); group II, albumin treatment (three doses of 1 g/kg 25% human albumin every 2 h); group III, endotoxin treatment with a single IV dose of 4 mg/kg endotoxin; and group IV, endotoxin and albumin-treatment (4 mg/kg endotoxin plus albumin treatment). Experiments lasted for 6 h while fluid intake was equally maintained in all groups.
  
  
  RESULTS
  COP and other variables were measured every 2 h. To determine the water content of an organ, after the rat was killed, the lung, heart, kidney, intestine, and liver were removed. Albumin treatment alone (group II) generated significant increases in COP (maximum, 58% from the baseline measurement) but did not change the water content of the organ, compared with saline solution-treated controls. Endotoxin-treated rats (group III) developed significant reductions in COP, with significant increases in pulmonary, renal, and heart water content compared with controls. Albumin treatment in endotoxemic rats (group IV) significantly increased the COP without improving the endotoxemia-induced organ edema. Pulmonary edema, however, was increased further, compared with endotoxemia alone.
  
  
  CONCLUSIONS
  COP elevation by albumin administration during the early stage of endotoxemia does not ameliorate pulmonary or multiple-organ edema and may aggravate pulmonary edema.
authors.affiliation: Division of Critical Care Medicine, Miami Children's Hospital, Miami, FL 33155-3009, USA.
authors.forename: M T
authors.initials: MT
authors.lastname: Camacho
authors.forename: B R
authors.initials: BR
authors.lastname: Totapally
authors.forename: D
authors.initials: D
authors.lastname: Torbati
authors.forename: J
authors.initials: J
authors.lastname: Wolfsdorf
mesh_terms: D000818:Animals; D001834:Body Water / Q000502:physiology*; D002199:Capillary Permeability; D002245:Carbon Dioxide / Q000097:blood; D003102:Colloids; D019446:Endotoxemia / Q000097:blood / Q000150:complications / Q000503:physiopathology*; D004731:Endotoxins; D004926:Escherichia coli; D006454:Hemoglobins / Q000032:analysis; D006874:Hydrostatic Pressure; D008297:Male; D009997:Osmotic Pressure; D010100:Oxygen / Q000097:blood; D011654:Pulmonary Edema / Q000209:etiology / Q000503:physiopathology*; D011659:Pulmonary Gas Exchange; D051381:Rats; D017207:Rats, Sprague-Dawley; D012709:Serum Albumin / Q000008:administration & dosage; D012965:Sodium Chloride / Q000008:administration & dosage; D014882:Water-Electrolyte Balance
chemical_list: D003102:Colloids; D004731:Endotoxins; D006454:Hemoglobins; D012709:Serum Albumin; D002245:Carbon Dioxide; D012965:Sodium Chloride; D010100:Oxygen