Response Of Skeletal Muscle Arterioles In Vivo To Modulation Of Endothelial Glycocalyx (Eg) By Resuscitation Fluids After Hemorrhagic Shock (Hs)

EG shedding may be associated with deleterious endothelial function, leading to edema, inflammation, poor vasomotor control and tissue hypoxia. Previous studies reported that fluid shear stress may stimulate glycocalyxsynthesis and modulate arteriolar diameter. Administration of resuscitation fluids in severely hemorrhaged patients may result in hemodilution, edema and impairment of microvascular perfusion. Therefore this study aims to elucidate the effects of such fluids on arteriolar glycocalyx and the overall hemodynamic response after HS followed by hypotensive resuscitation. Anesthetized rats (n=30) subjected to HS for 1h (25mL/kg blood loss) were resuscitated with fresh frozen plasma (FFP), fresh whole blood (FWB), 5% Albumin (ALB), lactated Ringer's (LR) or normal saline (NS). The volume infused was 15 mL/kg (FFP, FWB and ALB) or 45 mL/kg (LRor NS). In addition of systemic parameters, EG thickness, red cell velocity, blood flow, wall shear rate (WSR) and wall shear stress (WSS), as well as permeability were studied on over 30 arterioles using intravital microscopy. Post‐resuscitation arterial pressure was 20% lower than baseline in alltreated‐rats. Also post‐resuscitation hematocrit decreased equally to 24±1 % in all groups, except in FWB group (33±1 %). Arteriolar blood flow was significantly lower on rats treated with LR and NS compared to FFP, FWB and ALB treatments. After resuscitation, arteriolar WSR returned to baseline levels in all groups, however WSS was significantly lower in LR and NS compared to FFP, FWB and ALB. Arteriolar EG thickness was lower in LR and NS, whereas it recovered in FFP, FWB and ALB, compared to baseline (p<0.05). A linear correlation between changes in arteriolar diameter (relative to baseline) and changes in EG thickness (R=0.56, p<0.05) as well as changes in WSS (R=0.60, p<0.05)were observed. To conclude, as previously shown in venules, shedding/recovery of the EG occurs also within arterioles of the rat cremaster network. In addition, fluid resuscitation after HS may improve arteriolar EG recovery, endothelium function and microhemodynamics, possibly due to higher viscosity fluids that modulates shear stress and its effect on the endothelium, without volume overload. Support or Funding Information Supported by US Army Medical Research & Materiel Command