Rupture of an abdominal aortic aneurysm causes priming of phagocytic oxidative burst.
OBJECTIVE
The purpose of this investigation was to determine whether rupture and repair of an abdominal aortic aneurysm induced activation of phagocyte oxidant burst, reflecting a systemic inflammatory state, when compared with elective abdominal aortic aneurysm (AAA) repair.


METHODS
Blood samples were harvested from 22 patients with elective AAA and 15 patients with ruptured AAA. Phagocyte oxidant activity was measured in response to a panel of activators with luminol and lucigenin as chemiluminescent substrates. Activity of the complement pathways was measured with plasma levels of C3a des arg.


RESULTS
Elective AAA repair resulted in significant elevation in phagocyte count and oxidative activity after surgery in response to maximal dose phorbol myristate acetate (PMA) when compared with the baseline sample. In patients with ruptured AAA the oxidative activity of phagocytes was significantly increased in response to both unopsonized zymosan (899.8 +/- 192 ruptured vs 300 +/- 40 elective, p < 0.01) and maximal dose PMA (8769 +/- 2011 vs 3508 +/- 382, p < 0.01) compared with elective cases at the initial sampling. Phagocyte priming has occurred by way of two distinct pathways: receptor-mediated (unopsonized zymosan, CR3 receptor) and receptor-independent (PMA, protein kinase c).


CONCLUSIONS
Rupture of an AAA resulted in priming of the phagocyte oxidant capacity before operative repair compared with elective AAA. Phagocyte activation is a critical component of the systemic inflammatory response that may contribute to the high incidence of systemic organ dysfunction and death in this patient group.
Lindsay
T F
TF
Division of Vascular Surgery, Toronto Hospital, Ontario, Canada.
Memari
N
N
Ghanekar
A
A
Walker
P
P
Romaschin
A
A
D000166:Acridines; D000368:Aged; D000706:Anaphylatoxins / Q000032:analysis; D017544:Aortic Aneurysm, Abdominal / Q000097:blood / Q000473:pathology* / Q000601:surgery; D001019:Aortic Rupture / Q000097:blood / Q000473:pathology*; D002452:Cell Count; D015926:Complement C3a / Q000031:analogs & derivatives / Q000032:analysis; D003171:Complement Pathway, Classical; D017558:Elective Surgical Procedures; D006801:Humans; D007202:Indicators and Reagents; D008163:Luminescent Measurements; D008165:Luminol; D016177:Macrophage-1 Antigen / Q000378:metabolism; D010586:Phagocytes / Q000187:drug effects / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D011493:Protein Kinase C / Q000378:metabolism; D016897:Respiratory Burst; D018746:Systemic Inflammatory Response Syndrome / Q000209:etiology; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D015054:Zymosan / Q000494:pharmacology
D000166:Acridines; D000706:Anaphylatoxins; D007202:Indicators and Reagents; D016177:Macrophage-1 Antigen; C044541:complement C3a, des-Arg-(77)-; C033472:10,10'-dimethyl-9,9'-biacridinium; D008165:Luminol; D015926:Complement C3a; D015054:Zymosan; D011493:Protein Kinase C; D013755:Tetradecanoylphorbol Acetate