Increased Intestinal Permeability in Deceased Brain Dead Rats

Crosstalk between Complement and Toll-like Receptor Activation in Relation to Donor Brain Death and Renal Ischemia-Reperfusion Injury

“…As described previously, blocking C5 activation or the C5aR reduces renal IRI (13)(14)(15). In addition, improved graft survival was observed of mice kidneys treated with a C5aR inhibitor during preservation (69). Others showed improved long term graft survival in mice when recipients were treated with C5aR inhibitor before or even after transplantation (70).…”

Prednisolone has a positive effect on the kidney but not on the liver of brain dead rats: a potencial role in complement activation

“…Systemic production of circulating cytokines including interleukin-6 (IL-6), interleukin-10 (IL-10), Tumor Necrosis Factor-alpha (TNF- α ), Transforming Grown Factor-beta (TGF- β ) and Monocyte chemotactic protein 1 (MCP-1) are thought to orchestrate this response. The trigger for this inflammatory process is not well understood, however recent evidence suggests there could be a role for cerebral cytokines that cross the blood-brain barrier, in addition to complement activation [22,23] and intestinal bacterial translocation [24,25]. …”

Intestinal transplantation: The anesthesia perspective

“…Cold ischemic time (CIT) maybe directly related to structural graft quality [13]. There have been concerns regarding loss of intestinal tight junctions, which are essential to maintain the integrity of the intestinal barrier to prevent the translocation of toxins and bacteria [17]. However, no histological differences were observed in grafts with more and less than 9 h of CIT, therefore the 9-h cut-off cold ischemia time is debatable [13].…”