[Pathophysiologies of ischemic/reperfusion injuries associating with hemorrhagic shock and up-to-date treatment].
During the ischemic state, hypoxanthine and xanthine oxidase are accumulated in the ischemic cells, and thereafter when oxygen is reperfused into ischemic cells, hypoxanthine and xanthine oxidase work to change oxygen into oxygen radicals. Oxygen radicals themselves damage various cells and they also injure cells by activating the transcription factors of inflammatory cells to induce special protein synthesis depending on individual cells. These processes are considered to be related to the systemic inflammatory response syndrome (SIRS) and multiple-organ dysfunction syndrome (MODS). Hemorrhagic shock is a generalized ischemic state and intestinal ischemia is more profound and more severely damaging than in other vital organs because of luxurious flow to the latter organs. The lack of microcirculation in large areas of the intestinal mucosa and in high-density areas of intestinal immune cells results in the synthesis of various inflammatory mediators, in the appearance of adhesion molecules, in the induction of tissue factors, and finally in the development of impairment of remote vital organs and MODS when oxygen is reperfused. There is no therapy for reperfusion injury after a prolonged ischemic state, and thus it is most important to reduce the intestinal ischemic time by supplying sufficient oxygen to preserve intestinal circulation and to commence early enteral nutrition. The development of new treatments to interrupt the vicious pathological cascade inducing MODS after ischemic reperfusion injury is mandatory.
Shinozawa
Yotaro
Y
Department of Emergency and Critical Care Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.
Koike
Kaoru
K
D006801:Humans; D015427:Reperfusion Injury / Q000503:physiopathology* / Q000517:prevention & control / Q000628:therapy*; D012771:Shock, Hemorrhagic / Q000503:physiopathology* / Q000628:therapy*