Microcirculation and reperfusion injury in organ transplantation.
There are many interesting aspects regarding hemorheology and tissue oxygenation in organ transplantation (such as liver, kidney, heart, etc.). The ischemia-reperfusion injury syndrome is a very important problem. Much damage in organs appears to be induced by reperfusion injury syndrome. In fact, not only immunological etiopathogenesis but also biochemically-mediated microcirculation alterations can modulate the organ damage induced by ischemia-reperfusion injury during organ transplantation. During ischemia-reperfusion injury, xanthine oxidase activity, the increase in oxygen free-radicals, and the activation of neuthrophils are all very important. Platelet activating factor (PAT) and LTB4 (promoting neuthrophils adhesiveness), activated by the xanthine oxidase-derived oxidants during reperfusion, activates the final post-ischemia injury. Much research is necessary in order to gain a fuller knowledge of the microcirculation conditions and oxygenation during organ transplantation.
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Giuseppe
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D000328:Adult; D005260:Female; D006419:Heme Oxygenase (Decyclizing) / Q000378:metabolism; D018056:Hemorheology; D006801:Humans; D019194:Ischemic Preconditioning; D016031:Liver Transplantation / Q000009:adverse effects* / Q000502:physiology; D008297:Male; D008833:Microcirculation / Q000503:physiopathology*; D008875:Middle Aged; D008954:Models, Biological; D009569:Nitric Oxide / Q000378:metabolism; D012039:Regional Blood Flow; D015427:Reperfusion Injury / Q000209:etiology* / Q000503:physiopathology / Q000517:prevention & control; D013481:Superoxides / Q000378:metabolism
D013481:Superoxides; D009569:Nitric Oxide; D006419:Heme Oxygenase (Decyclizing)