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Table 2 Preclinical models of albumin

From: Role of albumin in the preservation of endothelial glycocalyx integrity and the microcirculation: a review

Preclinical modelMain findingsReference
Mechanism of action (MoA)
Rat perfused venular microvesselPrimary MoA of albumin in maintaining vascular permeability is release of S1P from RBCs[73]
Rat experimentally induced hypovolemic shockAlbumin infusion partially restored the measured thickness of the endothelial glycocalyx and restored microvascular permeability. Restored permeability may be due to delivery of S1P to the endothelium and not wholly dependent on glycocalyx recovery[74]
In vitro human uterine vein endothelial cells exposed to LPS and TNF-αHuman serum albumin (4%) inhibited inflammatory and oxidative stress pathways induced by endotoxins[75]
In vitro model of inflammatory vascular injury using bovine aortic endothelial cellsHuman serum albumin had modest intrinsic non-thiol-dependent anti-inflammatory effects[76]
In vitro artificial semipermeable membraneAlbumin decreased water permeability of ultrafiltration membranes in a concentration dependent manner. Effects were mediated by plugging of the capillary pore and solute–solvent exchange at the capillary membrane surface[77]
Atomic force microscopy and reflectance interference contrast microscopy of bovine lung endothelial cellsAlbumin (0.1% and 4%) increased the thickness and produced softening of the glycocalyx compared with 1% albumin. Albumin produced glycocalyx softening in a concentration-dependent manner[13]
Models of hemorrhagic shock
Anesthetized rats subjected to hemorrhagic shockAlbumin partially restored endothelial glycocalyx thickness and stabilized permeability and leukocyte rolling/adhesion[60]
Awake hamsters subjected to hemorrhagic shockAlbumin improved the microcirculation in correcting metabolic disorders (improving arterial base excess and oxygen extraction ratio) more effectively than RBC infusion[78]
Rat intravital microscopy of the mesenteric microcirculationAlbumin improved microcirculation and global hemodynamics following hemorrhagic shock and attenuated the inflammatory response to reperfusion[79]
Models of endotoxemia
Mouse experimentally induced endotoxemiaHuman serum albumin (4%) increased survival of endotoxemic mice compared with saline[75]
Rat experimentally induced endotoxemiaHuman serum albumin (4% or 20%) increased perfused vessel density and blood flow velocity and decreased flow heterogeneity to control values[80]
Rat experimentally induced endotoxemiaAlbumin (20%) improved hemodynamic parameters and microcirculatory perfusion; association with recovery of some glycocalyx components[81]
Models of vascular permeability
Ex vivo perfused isolated guinea pig heartHES infusion, but not albumin infusion, significantly decreased net coronary fluid filtration[82]
Rat experimentally induced hemorrhage or sepsisFollowing hemorrhage or cecal ligation and incision, plasma volumes after albumin or crystalloid infusions were similar[83]
Ex vivo perfused isolated guinea pig heartGlycocalyx integrity was maintained with 1% human albumin and crystalloid, but functional breakdown of the vascular barrier was observed with 0.5% albumin and crystalloid[84]
Rat anaphylactic shockUnder conditions of increased microvascular permeability, albumin (5%) was the most effective plasma volume expander compared with gelatin (4%), HES (6%) or saline[85]
Models of ischemia
Ex vivo perfused isolated guinea pig heartAlbumin was more effective than HES or saline in preventing cardiac fluid extravasation with ischemia–reperfusion injury[86]
Rat transient focal cerebral ischemiaCompared with saline, albumin reperfusion had a neuroprotective effect, significantly increasing arteriolar diameter and improving venular and capillary erythrocyte perfusion with increased erythrocyte flow velocity[87]
  1. HES hydroxyethyl starch; LPS lipopolysaccharide; MoA mechanism of action; RBC red blood cell; S1P sphingosine-1-phosphate; TNF-α tumor necrosis factor alpha