title: Does insulin impact cold-induced fluid- and protein-extravasation?
abstract: BACKGROUND
  Insulin has been shown to stabilize the endothelial barrier via inactivation of the endothelial contractile machinery and enhancement of cell-cell adhesions. Here we explored if insulin by its endothelial-stabilizing and anti-inflammatory properties could influence the increase of fluid- and protein-extravasation during hypothermia.
  
  
  METHODS
  Two groups of animals (n=10, each) were cooled to 28°C, with insulin-infusion (I-group) or without (C-group), in a randomly controlled study. Fluid balance, hemodynamics, plasma volume (PV), colloid osmotic pressures in plasma (COPp) and interstitial fluid (COPi), hematocrit (Hct), cytokine profiles, serum-albumin- and protein-concentrations were measured and fluid extravasation rate (FER) and albumin-and protein-masses calculated.
  
  
  RESULTS
  During 240 min of hypothermia the albumin- and protein-masses together with COPp decreased significantly in both groups. COPi remained essentially unchanged. Plasma volume decreased significantly in the C-group, whereas only a decreasing trend was present in the I-group. Hemoconcentration was significant in both study groups reflected by the Hct-values. A slight increasing trend of FER was seen in both groups from 0.10 (0.04) ml/kg/min and 0.09 (0.05) mg/kg/min, C-group and I-group, respectively, to 0.14 (0.05) mg/kg/min and 0.12 (0.03) mg/kg/min, during the hypothermic period. Between-group differences were absent for all listed parameters including FER.
  
  
  CONCLUSIONS
  Insulin administration does not impact fluid and protein extravasation significantly in animals undergoing cooling and prolonged hypothermia.
authors.affiliation: Department of Anesthesia and Intensive Care, Haukeland University Hospital, 5021 Bergen, Norway. Electronic address: hege.kristin.brekke@helse-bergen.no.
authors.forename: Hege K
authors.initials: HK
authors.lastname: Brekke
authors.affiliation: Department of Anesthesia and Intensive Care, Haukeland University Hospital, 5021 Bergen, Norway.
authors.forename: Stig
authors.initials: S
authors.lastname: Hammersborg
authors.affiliation: Department for Hyperbaric Medicine, Haukeland University Hospital, 5021 Bergen, Norway.
authors.forename: Torbjørn
authors.initials: T
authors.lastname: Nedrebø
authors.affiliation: Department of Clinical Medicine, University of Bergen, 5021 Bergen, Norway.
authors.forename: Paul
authors.initials: P
authors.lastname: Husby
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000378:metabolism; D002199:Capillary Permeability; D002448:Cell Adhesion; D004727:Endothelium / Q000502:physiology; D006439:Hemodynamics / Q000502:physiology*; D007035:Hypothermia / Q000503:physiopathology*; D007036:Hypothermia, Induced / Q000662:veterinary*; D007328:Insulin / Q000378:metabolism / Q000494:pharmacology*; D008297:Male; D009997:Osmotic Pressure / Q000502:physiology; D010953:Plasma Volume / Q000502:physiology; D012709:Serum Albumin / Q000502:physiology; D034421:Sus scrofa; D019108:Tight Junctions; D014882:Water-Electrolyte Balance / Q000187:drug effects* / Q000502:physiology
chemical_list: D000893:Anti-Inflammatory Agents; D007328:Insulin; D012709:Serum Albumin
keywords: Endothelial barrier function; Fluid shifts; Hypothermia; Inflammation; Insulin