Discussion
tissue injury, traumatic hemorrhagic shock, death, ischemia
PATHOLOGICAL PROCESS, EVENTS, OXIDATIVE STRESS, ISCHEMIA
Dysregulated immuno-inflammatory responses may contribute to adverse outcomes following traumatic hemorrhagic shock despite successful resuscitation protocolsIschemia/reperfusion injury is a pathological process caused by tissue ischemia followed by restoration of perfusion, which together initiate a cascade of cellular events culminating in the tissue injury due to the generation of oxidative stress, initiation of the cell death pathways and generation of pro-inflammatory moleculesIn addition to degranulation, activated neutrophils have also been shown to secrete VEGFIn our investigation of a panel of cytokines/chemokines, we observed that RIC prevented the significant increases in the cytokines MDC/CCL22 and TARC/CCL17 at 24 h post intervention. Both MDC and TARC are specific ligands for C–C chemokine receptor type 4, a receptor expressed on myeloid cells and lymphocytes but predominately on Th2 cellsSeveral studies in humans have sought to determine the potential mediators of RIC and have measured a number of humoral and immunomodulatory molecules, including plasma levels of cytokines, hormones, and factors