Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-4503
Ganter, M T; Cohen, M J; Brohi, K; Chesebro, B B; Staudenmayer, K L; Rahn, P; Christiaans, S C; Bir, N D; Pittet, J F (2008). Angiopoietin-2, marker and mediator of endothelial activation with prognostic significance early after trauma. Annals of Surgery, 247(2):320-326.
OBJECTIVE: To measure plasma levels of angiopoietin-1 (Ang-1), angiopoietin-2 (Ang-2), and vascular endothelial growth factor (VEGF) early after trauma and to determine their clinical significance. BACKGROUND: Angiopoietins and VEGF play a central role in the physiology and pathophysiology of endothelial cells. Ang-2 has recently been shown to have pathogenetic significance in sepsis and acute lung injury. Little is known about the role of angiopoietins and VEGF early after trauma. METHODS: Blood specimens from consecutive major trauma patients were obtained immediately upon arrival in the emergency department and plasma samples assayed for Ang-1, Ang-2, VEGF, markers of endothelial activation, protein C pathway, fibrinolytic system, and complement. Base deficit was used as a measure of tissue hypoperfusion. Data were collected prospectively. RESULTS: Blood samples were obtained from 208 adult trauma patients within 30 minutes after injury before any significant fluid resuscitation. Plasma levels of Ang-2, but not Ang-1 and VEGF were increased and correlated independently with severity of injury and tissue hypoperfusion. Furthermore, plasma levels of Ang-2 correlated with markers of endothelial activation, coagulation abnormalities, and activation of the complement cascade and were associated with worse clinical outcome. CONCLUSIONS: Ang-2 is released early after trauma with the degree proportional to both injury severity and systemic hypoperfusion. High levels of Ang-2 were associated with an activated endothelium, coagulation abnormalities, complement activation, and worse clinical outcome. These data indicate that Ang-2 is a marker and possibly a direct mediator of endothelial activation and dysfunction after severe trauma.
|Item Type:||Journal Article, refereed, original work|
|Communities & Collections:||04 Faculty of Medicine > University Hospital Zurich > Institute of Anesthesiology|
|DDC:||610 Medicine & health|
|Deposited On:||21 Oct 2008 10:48|
|Last Modified:||27 Nov 2013 17:53|
|Publisher:||Lippincott Wiliams & Wilkins|
|Citations:||Web of Science®. Times cited: 42|
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