Cytokine balance in hepatosplanchnic system during thoracoabdominal aortic aneurysm repair

Abstract

While prolonged visceral ischemia seems to be a potential source of elevated proinflammatory cytokines during thoracoabdominal aortic aneurysm (TAAA) repair, the underlying mechanisms are unclear. We have investigated the production of cytokines and fatty acid binding proteins (FABPs) in the hepatosplanchnic system during TAAA repair. Arterial and hepatic venous levels of tumor necrosis factor-alpha (TNF-α), interleukin (IL) -6, -8, and -10, and liver- and intestinal-type FABPs (L-FABP, I-FABP) were measured at four time points in ten patients undergoing TAAA repair. Visceral arteries were perfused through either a side-arm of distal aortic perfusion or an individual circuit using an independent pump, or both, without measuring perfusion pressure or blood flow. The postoperative courses of all patients were uneventful. During visceral perfusion, the levels of arterial IL-6, -8, and -10, and L-FABP elevated significantly (P=0.0077, 0.0051, 0.0077, 0.0077, respectively), and these elevated levels persisted up to skin closure, with the exception of L-FABP (P=0.0051 each). In contrast, there were only subtle increases in TNF-α and I-FABP levels. The production ratio through the hepatosplanchnic system of TNF-α, L-FABP, and I-FABP showed a pronounced peak during visceral perfusion, but only the peak of L-FABP was significant compared with baseline (P=0.0077). All production ratios returned to baseline level at skin closure. The production ratio of IL-6 was negative throughout the operation and that of IL-8 and IL-10 remained at baseline during visceral perfusion. In conclusion, a portion of the TNF-α, L-FABP, and I-FABP might be produced temporarily in the hepatosplanchnic system during TAAA repair. Systemic elevation of IL-6, IL-8, and IL-10 might be modulated by inflammatory response to extracorporeal circulation or surgical stress. Thus, our simple visceral perfusion techniques may indeed be justified.