Systemic endothelial activation is greater in septic than in traumatic-hemorrhagic shock but does not correlate with endothelial activation in skin biopsies.
OBJECTIVE
Sepsis and severe trauma result in endothelial activation and damage. The activated endothelium expresses adhesion receptors that control leukocyte trafficking. After activation, some adhesion molecules are also released into plasma as soluble forms. The present study was designed to compare the expression of soluble cell adhesion molecules (sCAMs) in three groups of patients: those with septic shock, severe sepsis, and traumatic-hemorrhagic shock. In addition, the endothelial expression of these adhesive molecules was examined in skin biopsies.


METHODS
Prospective observational study


METHODS
Intensive care unit at a university hospital


METHODS
The study included 15 patients with septic shock (by Bone's definition), 11 patients with severe sepsis (by Bone's definition), and 13 patients with traumatic-hemorrhagic shock. Fifteen healthy blood donors served as controls.


RESULTS
Measurements of sCAMs were performed on days 1, 2, and 3 of the disease. On day 1, when compared with controls, sE-selectin, sP-selectin, soluble vascular cell adhesion molecule (sVCAM)-1, and soluble intercellular adhesion molecule (sICAM)-1 were markedly elevated in septic shock patients, whereas these sCAMs, except for sP-selectin, were within normal ranges in traumatic-hemorrhagic shock patients. In patients with severe sepsis, an earlier stage than septic shock in the sepsis continuum, intermediate values of sCAMs were found. In skin biopsies of septic shock patients, the endothelial cells expressed a bright staining of constitutive endothelial molecules (CD146, CD144, CD131). Inducible molecules (ICAM-1, VCAM-1, and E-selectin) were positively expressed with bright staining. The biopsies from traumatic-hemorrhagic shock patients showed a similar positive expression of endothelial molecules.


CONCLUSIONS
The patterns of sCAMs indicate that the systemic activation of the endothelium is different in the three clinical entities, maximum in septic shock, intermediate in severe sepsis, and not different from controls in traumatic-hemorrhagic shock. Comparable endothelial activation as evidenced by skin biopsies suggests that caution is required in the interpretation of CAMs in plasma, which does not necessarily reflect the in situ activation state of endothelium.
Leone
Marc
M
Intensive Care Unit and Trauma Center, Unité des Rickettsies, CNRS UMR 6020, France.
Boutière
Brigitte
B
Camoin-Jau
Laurence
L
Albanèse
Jacques
J
Horschowsky
Nicole
N
Mège
Jean-Louis
JL
Martin
Claude
C
Dignat-George
Françoise
F
D000328:Adult; D015703:Antigens, CD; D051929:CD146 Antigen; D015815:Cell Adhesion Molecules / Q000032:analysis; D016207:Cytokines / Q000032:analysis; D019040:E-Selectin / Q000032:analysis; D004727:Endothelium / Q000502:physiology*; D005260:Female; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis; D008297:Male; D008562:Membrane Glycoproteins; D008875:Middle Aged; D019006:Neural Cell Adhesion Molecules; D019007:P-Selectin / Q000032:analysis; D011446:Prospective Studies; D011956:Receptors, Cell Surface / Q000032:analysis; D012771:Shock, Hemorrhagic / Q000503:physiopathology*; D012772:Shock, Septic / Q000503:physiopathology*; D012774:Shock, Traumatic / Q000503:physiopathology; D012867:Skin / Q000737:chemistry; D019010:Vascular Cell Adhesion Molecule-1
D015703:Antigens, CD; D051929:CD146 Antigen; D015815:Cell Adhesion Molecules; D016207:Cytokines; D019040:E-Selectin; C497902:MCAM protein, human; D008562:Membrane Glycoproteins; D019006:Neural Cell Adhesion Molecules; D019007:P-Selectin; D011956:Receptors, Cell Surface; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1