Blood-Graft Interactions: With special reference to cellular immune-reactivity in vascular and endovascular surgery

Sammanfattning: The expression of surface adhesion molecules on white blood cells (WBC) and platelets, and the release of tumor necrosis factor-alpha (TNF-a) and interleukin-6 (IL-6) after incubation with expanded-polytetrafluoroethylene (ePTFE)- or woven Dacron grafts was determined. Both graft-materials induced alteration of the WBC adhesion molecule receptor and caused release of TNF-a and IL-6, higher for woven Dacron as compared to ePTFE. The expression of platelet surface antigens was less evidently influenced. Two anti-inflammatory drugs demonstrated to significantly reduce the release of TNF-a and IL-6. The light microscopic appearance by nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase as well as factor VIII in endothelial cells (EC), lining the graft-surface during healing of stretch-ePTFE arterial grafts in porcine experiments, demonstrated a lower expression of NADPH-d and factor VIII compared to native EC. This may reflect immature EC and probably a decreased expression of nitric oxide (NO). An early inflammatory response was recorded in patients undergoing aorto-bifemoral bypass surgery with a release of IL-6 and C-reactive protein, but not TNF-a. The complement proteins varied their patterns with C1q depletion and C5a increase, interpreted as a complement activation. A corresponding methodology was used to study patients undergoing implantation of an endoluminal device, compared to conventional surgery for abdominal aortic aneurysms. During endovascular repair a majority of patients suffered a blood pressure decrease when the device was introduced. Further, a significant inflammatory response, mainly involving TNF-a was induced. Cell activation caused by the aneurysmal content could possibly explain the findings. Responses were confirmed by determination of surface adhesion molecule receptors on both circulating and sequestered WBC. Conventional repair induced responses related to the more extensive surgical trauma. To conclude, certain differences regarding acute cellular immune reactivity during vascular and endovascular surgery were demonstrated, mediated by surface adhesion molecules, various cytokines, and complement proteins.