Therapeutic modulation of free radical-mediated reperfusion injury of the liver and its surgical implications.
It is well known that ischemia causes functional and structural damage to liver cells, and that the status of energy metabolism provides an important means of assessing the functional viability of the ischemic organ. However, the specific sequence leading to ischemic liver cell injury is not yet fully understood; therefore, it is clinically and pathophysiologically important to elucidate the mechanism of cellular injury during hepatic ischemia and subsequent reperfusion. Whereas the conventional view attributes this injury process to the ischemia itself, recent studies have demonstrated that a variable but often substantial proportion of this injury is caused by reactive oxygen metabolites that are generated at the time of reperfusion. This article presents an outline of the mechanism of cellular injury caused during hepatic ischemia and subsequent reperfusion resulting from certain types of surgery, with special reference to the xanthine-xanthine oxidase system and the activation of neutrophils and macrophages.
Marubayashi
S
S
Department of Surgery, Hiroshima University School of Medicine, Japan.
Dohi
K
K
D000818:Animals; D015815:Cell Adhesion Molecules; D005609:Free Radicals; D006801:Humans; D008099:Liver / Q000098:blood supply* / Q000601:surgery; D016031:Liver Transplantation; D008262:Macrophage Activation; D018375:Neutrophil Activation; D017382:Reactive Oxygen Species; D015427:Reperfusion Injury / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D019820:Xanthine; D014969:Xanthine Oxidase / Q000502:physiology; D014970:Xanthines / Q000378:metabolism
D015815:Cell Adhesion Molecules; D005609:Free Radicals; D017382:Reactive Oxygen Species; D014970:Xanthines; D019820:Xanthine; D014969:Xanthine Oxidase