Preclinical model | Main findings | Reference |
---|---|---|
Mechanism of action (MoA) | ||
Rat perfused venular microvessel | Primary MoA of albumin in maintaining vascular permeability is release of S1P from RBCs | [73] |
Rat experimentally induced hypovolemic shock | Albumin 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-α | Human serum albumin (4%) inhibited inflammatory and oxidative stress pathways induced by endotoxins | [75] |
In vitro model of inflammatory vascular injury using bovine aortic endothelial cells | Human serum albumin had modest intrinsic non-thiol-dependent anti-inflammatory effects | [76] |
In vitro artificial semipermeable membrane | Albumin 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 cells | Albumin (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 shock | Albumin partially restored endothelial glycocalyx thickness and stabilized permeability and leukocyte rolling/adhesion | [60] |
Awake hamsters subjected to hemorrhagic shock | Albumin 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 microcirculation | Albumin improved microcirculation and global hemodynamics following hemorrhagic shock and attenuated the inflammatory response to reperfusion | [79] |
Models of endotoxemia | ||
Mouse experimentally induced endotoxemia | Human serum albumin (4%) increased survival of endotoxemic mice compared with saline | [75] |
Rat experimentally induced endotoxemia | Human serum albumin (4% or 20%) increased perfused vessel density and blood flow velocity and decreased flow heterogeneity to control values | [80] |
Rat experimentally induced endotoxemia | Albumin (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 heart | HES infusion, but not albumin infusion, significantly decreased net coronary fluid filtration | [82] |
Rat experimentally induced hemorrhage or sepsis | Following hemorrhage or cecal ligation and incision, plasma volumes after albumin or crystalloid infusions were similar | [83] |
Ex vivo perfused isolated guinea pig heart | Glycocalyx 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 shock | Under 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 heart | Albumin was more effective than HES or saline in preventing cardiac fluid extravasation with ischemia–reperfusion injury | [86] |
Rat transient focal cerebral ischemia | Compared 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] |