After ischemia/reperfusion injury, complement is activated via all three established pathways (classical, alternative and MBL) (95) (96) (97) . Endothelium damaged by hypoxic stress activates complement, leading to elevated vascular permeability, release of anaphylatoxins and the accumulation of neutrophils (98) . Experimental studies indicated complement activation after ischemia/reperfusion in several organs, including lung, liver, gut, kidney, myocardium and skeletal muscle (99) (100) (101) (102) (103) (104) (105) .