Peripheral Vascular Surgery Society

#4 ELECTIVE AND RUPTURED ABDOMINAL AORTIC ANEURYSM REPAIR DELAYS PMN APOPTOSIS.

William S. Johnson, BSc, Rohan Shahani, MSc, Barry B. Rubin, MD,

Paul M. Walker, MD, and Thomas F. Lindsay, MD

The Toronto Hospital, Toronto, Ontario, Canada

Rupture of an abdominal aortic aneurysm (RAAA) is a lethal event associated with 40-70% mortality. Postoperative multi-organ dysfunction syndrome (MODS), which is related to the presence of activated PMNs is responsible for up to 50% of the mortality. A delay in PMN apoptosis will result in the persistence of activated PMNs. This may play a role in the development of tissue and organ injury. We hypothesized that the lower-torso ischemia/reperfusion of elective abdominal aortic aneurysm (EAAA) repair would delay PMN apoptosis. Hemorrhagic shock seen in RAAA may exaggerate the apoptotic delay and contribute to the development of MODS. Serial blood samples were taken from EAAA (n=5) and RAAA (n=3) patients. PMNs were isolated using dextran sedimentation and Ficoll gradient centrifugation. After 24 hours of incubation, PMNs were stained with hypotonic propidium iodide and the apoptotic rates measured as the percentage of PMNs with hypodiploid DNA by flow cytometry. An automated differential blood count was performed on each sample.

Group

EAAA RAAA

Sample Point Apoptosis Phagocyte Count Apoptosis Phagocyte Count

(% total PMNs) (x109/L) (% total PMNs) (x109/L)

PI 36.8±6.19 5.90±0.46 20.1±72† 3.3±3.00

PR 30.7±11.2* 6.57±0.66 13.4±2.08+ 5.87±0.70

2PR 18.4±4.92* 9.93±2.05‡ 14.8±0.83+ 7.91±1.04

4PR 11.9±1.66* 10.5±1.36‡ 12.6±1.87+ 7.54±1.10

Day 1 17.9±8.61* 12.1±1.26‡ 6.7±1.80+ 8.30±1.96

Day 2 16.4±1.74* 13.1±0.91‡ 11.4±2.45+ 9.30±2.25

Day 3 23.9±6.78 8.50±2.64 14.0±4.13+ 7.93±1.61

Day 4 18.6±3.67* 8.33±2.56 23.95 6.08±0.75

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PI= pre-incision, PR= pre clamp release, 2PR= 2 hours post clamp release, 4PR= 4 hours post clamp release, *p<0.05 vs. PI in EAAA group. +p<0.05 vs. PI in RAAA group. †p<0.05 vs. PI in EAAA group. ‡p<0.05 vs. PI in EAAA group.

In EAAA patients, PMN apoptosis was delayed at PR, 2PR, 3PR, Day 1, Day 2, and Day 4 when compared to the pre-incision sample. An inverse trend was observed in the numbers of circulating phagocytes with significant elevations at 2PR, 4PR, Day 1 and Day 2. RAAA's had an exaggerated delay in PMN apoptosis, noted at PI when compared to the EAAA group (p<0.05). We conclude that PMN apoptosis is delayed in both EAAA and RAAA repair. The increase in postoperative phagocyte number may be partly accounted for by the apoptotic delay. RAAA patients exhibit a greater initial differential delay in PMN apoptosis, related to the hemorrhagic shock that precedes aneurysm repair. This is an indication that shock alters PMN function prior to surgical intervention. We suspect that a reduction in PMN apoptosis contributes to the development of progressive organ injury following RAAA repair.

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Last updated January 1,2000