Please see Bibliography of References for a list of abstracts, manuscripts and posters.
L’Her E, Goetghebeur D, Tonnelier J, Gut-Gobert C, Boumediene A, Renault A, Boles J. Int Care Med. 2005;31(Supp 1):S43. Abstract 153.
Introduction: Endothelial function is depressed during sepsis, which in turn interacts with the proinflammatory response. If the rhAPC anticoagulatory effects have been extensively characterized, there are few studies analyzing its microcirculatory actions. Our aims were to evaluate endothelial function variations during sepsis and to investigate the microcirculatory effects of rhAPC.
Methods: Endothelial function was assessed using near-infrared spectrophotometry (InSpectra™, Hutchinson). Measurements were performed during the early management (H0) and during the subsequent 48 hours (H8-H24 and H24-H48). The study was approved by our local ethics committee.
Results: 38 patients were monitored (age 57±18; SAPSII 60±23), of which 10 without sepsis (control), 28 severe sepsis, and 22 septic shock. They were compared to 6 healthy volunteers (normal). Endothelial function was depressed during sepsis but septic shock was associated to more severe alteration (p<0.05). From the septic shock patients who received rhAPC (n+10), a "normal" endothelial function was restored in 50% cases (see figure). These improvements were not observed within septic patients without rhAPC.
Conclusion: These results confirm that endothelial dysfunction occurs during severe sepsis and that during septic shock, rhAPC infusion had microcirculatory effects within the first 48hrs of infusion.