Hypertonic saline dextran attenuates leukocyte accumulation in the liver after hemorrhagic: Shock and resuscitation

Background: Hemorrhagic shock and resuscitation triggers a global ischemia/reperfusion phenomenon, in which activated leukocytes are considered strong contributors to the ensuing tissue damage. Methods: The aim of the study was to investigate the effects of hypertonic saline dextran (HSD) on the early leukocyte/endothelial interactions (intravital fluorescence microscopy) in a rat model of hemorrhagic shock (1 hour at mean arterial pressure of 40 mm Hg), The resuscitation was performed with lactated Ringer's solution (RL, four times shed blood/20 minutes, n = 6), 6% dextran 60 (DEX, 100% shed blood/5 minutes, n = 8), and 7.2% NaCl/10% dextran 60 (HSD, 10% shed blood/2 minutes, n = 8), Results: After 1 hour of resuscitation, shock-induced stasis/adherence of leukocytes was further enhanced with RL (sinusoids 17.6 +/- 6.9%; venules 33.9 +/- 8.5%), whereas DEX and HSD attenuated leukocyte stagnation in sinusoids (DEX -7.4 +/- 6,1%; HSD -14.7 +/- 2.9%, p < 0.01 vs. RL) and leukocyte adherence in postsinusoidal venules (DEX -12.2 +/- 8.6%, p < 0.05 vs, RL; HSD -27 +/- 7.4%,p < 0.01 vs, RL), Conclusion: HSD reduced significantly the number of leukocytes accumulated in the liver after resuscitation of hemorrhagic shock, probably due to a combination of mechanisms of both components.