title: Utilization of extracorporeal membrane oxygenation alleviates intestinal ischemia-reperfusion injury in prolonged hemorrhagic shock animal model.
abstract: Intestinal ischemia-reperfusion injury is one of the main factors leading to multiple organ failure after resuscitation of prolonged hemorrhagic shock; however, the current conventional fluid resuscitation still cannot effectively reduce intestinal injury caused by prolonged hemorrhagic shock. To investigate the effect of ECMO resuscitation on alleviating intestinal ischemia-reperfusion injury in a prolonged hemorrhagic shock rabbit model. Thirty New Zealand white rabbits were randomly divided into three groups: control group, conventional fluid resuscitation group, and ECMO resuscitation group. The prolonged hemorrhagic shock model was established by keeping the arterial blood pressure from 31 to 40 mmHg for 3 h through the femoral artery bleeding, and performing the resuscitation for 2 h by conventional fluid resuscitation and ECMO resuscitation, respectively. Chiu's score of intestinal injury, serum lactate and TNF-α levels, intestinal mucosamyeloperoxidase (MPO) activity, intercellular adhesion molecule (ICAM-1), and Claudin-1expression were detected. The mean arterial blood pressure in Group 2 was significantly higher after resuscitation than in Group 1, but serum lactate and inflammatory cytokines TNF-α level were significantly lower. And Chiu's score of intestinal injury and myeloperoxidase (MPO) activity level and ICAM-1 expression were significantly lower in the ECMO resuscitation group, in which the Claudin-1 levels were significantly increased. ECMO resuscitation for the prolonged hemorrhagic shock improves tissue perfusion and reduces the systemic inflammation, and thus alleviates intestinal damage caused by prolonged hemorrhagic shock.
authors.affiliation: Department of Cardiovascular Surgery, Xinqiao Hospital, Third Military Medical University, 400037, Chongqing, China.
authors.forename: Liang
authors.initials: L
authors.lastname: Zhao
authors.forename: Lin
authors.initials: L
authors.lastname: Luo
authors.forename: Jinjin
authors.initials: J
authors.lastname: Chen
authors.forename: Juan
authors.initials: J
authors.lastname: Xiao
authors.forename: Weikun
authors.initials: W
authors.lastname: Jia
authors.forename: Yingbin
authors.initials: Y
authors.lastname: Xiao
mesh_terms: D000818:Animals; D001794:Blood Pressure; D062445:Claudin-1 / Q000378:metabolism; D004195:Disease Models, Animal; D015199:Extracorporeal Membrane Oxygenation; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000503:physiopathology; D019344:Lactic Acid / Q000097:blood; D008297:Male; D009195:Peroxidase / Q000378:metabolism; D011817:Rabbits; D015427:Reperfusion Injury / Q000150:complications / Q000473:pathology / Q000628:therapy*; D012720:Severity of Illness Index; D012771:Shock, Hemorrhagic / Q000150:complications / Q000473:pathology*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D062445:Claudin-1; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D019344:Lactic Acid; D009195:Peroxidase