Abstract

Introduction: Hypertonic saline (HS) shrinks endothelial cells thereby opening inter-endothelial gaps which may increase permeability. This increase in permeability is not supported by clinical studies suggesting that water is pulled into the vascular space not lost into the interstitium. We hypothesized that albumin influences the trans-endothelial fluid due to tonicity and HS by a mechanism other than oncotic pressure. Methods: Hydraulic permeability (Lp) was measured in rat mesenteric venules using the Landis micro-occlusion model. The effect of albumin on tonicity was tested by measuring Lp after successive perfusions with a 1% albumin/Ringers solution of varying sodium chloride (NaCl) concentrations (85, 135, 185, and 235 mM) (n = 6). To examine the effect of albumin with HS, additional venules were perfused with 1% albumin/Ringers ([NaCl] = 135 mM) and measures of Lp obtained after a subsequent perfusion with 1% albumin in 7% NaCl (n = 6). Results were compared to data from similar studies conducted without albumin. Units for Lp are x10−8 cm · sec−1 cm·H2O−1. Results: Fig. 1 shows the effect of varying the NaCl concentration on Lp with and without albumin. The ∗ signifies a difference as compared to the No Albumin group, p < 0.05. Fig. 2 shows a 3-fold decrease in Lp with 7% HS plus albumin as compared to 7% HS alone, p = 0.02. Conclusions: Albumin decreased Lp at higher concentrations of NaCl. Since this model controls for oncotic pressure, albumin may impact Lp by a mechanism other than oncotic force. HS shrinks endothelial cells that may widen intercellular gaps thereby potentially increasing permeability. However, albumin appears to stabilize the endothelial barrier during HS perfusion and prevents the loss of intravascular fluid. Appropriate albumin levels may play an important clinical role in modulating trans-endothelial fluid flux with HS.

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