The inflammatory response to vascular surgery-associated ischaemia and reperfusion in man: effect on postoperative pulmonary function.
OBJECTIVE
To characterise the inflammatory response to vascular surgery and ischaemia/reperfusion (I/R) in man, regarding release of inflammatory mediators, recruitment and activation of neutrophils, and their relation to postoperative pulmonary function.


METHODS
Prospective cohort study.


METHODS
Circulating neutrophil counts and plasma levels of elastase-alpha 1-antitrypsin (AT), a neutrophil degranulation product, were measured before and approx. 2.5 h (group 1, n = 19) after elective abdominal aortic surgery, and approx. 2.9 h after elective peripheral vascular surgery (group 2, n = 6), together with concentrations of neutrophil agonists, including activated complement (C3a), secretory phospholipase A2 (sPLA2), tumor necrosis factor (TNF-alpha), interleukin (IL)-6, IL-8 and granulocyte colony-stimulating factor (G-CSF). At the time of blood sampling, respiratory variables allowing computation of the lung injury score (LIS) were obtained in patients admitted after surgery in the intensive care unit (ICU), i.e. all group 1 patients and one group 2 patient.


RESULTS
Median (range) neutrophil counts rose by 80% (-28-208) and 90% (10-147) in groups 1 and 2, respectively (n.s. between groups). The increase (p < 0.05) in elastase-alpha 1-AT level was 121% (-5-439) in group 1 and 82% (18-792) in group 2 (n.s. between groups). There was a rise (p < 0.05) in C3a level by 93% (-42-751) and of sPLA2 level by 68% (-40-1400) after surgery for the groups together (n.s. between groups), and the rise of the elastase-alpha 1-AT related to that of the C3a levels. IL-6 and G-CSF concentrations increased more in group 1 than 2. The IL-8 concentration increased in group 1 only, and TNF-alpha was unchanged in all groups. In ICU patients, the LIS related to the postoperative rise in IL-6 level only, even though the rise in plasma concentrations of cytokines interrelated. No patient developed ARDS and all survived.


CONCLUSIONS
Vascular surgery and I/R in man activates complement, releases cytokines (except for TNF-alpha), and induces neutrophil recruitment and degranulation, which may primarily depend on complement activation. In contrast to the latter, the release of cytokines may depend on the extent of I/R and may contribute to transient pulmonary dysfunction after extensive I/R.
Groeneveld
A B
AB
Department of Internal Medicine, Free University Hospital, Amsterdam, The Netherlands.
Raijmakers
P G
PG
Rauwerda
J A
JA
Hack
C E
CE
D000328:Adult; D000368:Aged; D001012:Aorta, Abdominal / Q000601:surgery; D015926:Complement C3a / Q000032:analysis; D005260:Female; D016179:Granulocyte Colony-Stimulating Factor / Q000097:blood; D006438:Hemodilution; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood; D007866:Leg / Q000098:blood supply; D007958:Leukocyte Count; D019272:Leukocyte Elastase / Q000032:analysis; D008171:Lung Diseases / Q000097:blood / Q000209:etiology*; D008297:Male; D008875:Middle Aged; D009504:Neutrophils; D010741:Phospholipases A / Q000097:blood; D054467:Phospholipases A2; D011446:Prospective Studies; D015427:Reperfusion Injury / Q000097:blood* / Q000209:etiology; D015656:Respiratory Mechanics; D014168:Transferrin / Q000032:analysis; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D014656:Vascular Surgical Procedures / Q000009:adverse effects*; D000515:alpha 1-Antitrypsin / Q000032:analysis
D018836:Inflammation Mediators; D015850:Interleukin-6; D014168:Transferrin; D014409:Tumor Necrosis Factor-alpha; D000515:alpha 1-Antitrypsin; C037741:alpha 1-antitrypsin-leukocyte elastase complex; D016179:Granulocyte Colony-Stimulating Factor; D015926:Complement C3a; D010741:Phospholipases A; D054467:Phospholipases A2; D019272:Leukocyte Elastase