Original Article—Alimentary Tract

Journal of Gastroenterology

, Volume 45, Issue 11, pp 1103-1110

First online:

Induction of intestinal ischemia reperfusion injury by portal vein outflow occlusion in rats

  • Marco VincentiAffiliated withDepartment of Surgery, Division of Transplantation, University of California
  • , Matthias BehrendsAffiliated withDepartment of Anesthesia and Perioperative Care, University of California
  • , Kim DangAffiliated withStanford University School of Medicine
  • , Yeon H. ParkAffiliated withDepartment of Surgery, Gachon Medical School, Gil Medical Center
  • , Ryutaro HiroseAffiliated withDepartment of Surgery, Division of Transplantation, University of California
  • , Annabel Blasi-IbanezAffiliated withServei d’ Anestesiologia i Reanimacio, Hospital Clinic
  • , Tao LiuAffiliated withDepartment of Surgery, Division of Transplantation, University of California
  • , Natalie J. SerkovaAffiliated withDepartment of Anesthesiology, Biomedical MRI/PET/CT Cancer Center Core, University of Colorado Health Sciences Center
  • , Claus U. NiemannAffiliated withDepartment of Surgery, Division of Transplantation, University of CaliforniaDepartment of Anesthesia and Perioperative Care, University of California Email author 

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Intestinal ischemia can occur from mesenteric artery (MA) occlusion and portal vein (PV) occlusion. The degree and mechanisms of ischemia/reperfusion (I/R) injury in these conditions may differ. Metabolic changes are seen early in I/R. This study compares tissue histology, inflammation, and metabolic response during small bowel I/R due to superior MA or PV occlusion.


Anesthetized male Wistar rats (250–300 g) underwent laparotomy followed by MA or PV occlusion for 40 min. After 120 min of reperfusion, small bowel tissue was collected. The expression of heat shock protein (HSP)-32 and HSP70 was evaluated to compare physiological stress responses between groups. Metabolic profiles were obtained using 1H-nuclear magnetic resonance spectroscopy (NMR)-based quantitative metabolomics. Histological injury of small bowel was graded from 0 (normal) to 4 (extensive ischemic damage).


Protein expression of HSP32 and HSP70 increased when compared to sham but was not different in the MA I/R and PV I/R groups. Metabolic profiles demonstrated decreased glucose levels and highly elevated tissue lactate and amino acids and fatty acids following I/R, with more pronounced changes with PV occlusion. Lipid peroxidation was equally increased in both groups, while depletion of reduced glutathione (GSH) was more severe with MA occlusion. The epithelial necrosis score was higher with MA (3.5 ± 0.6) than with PV occlusion (2.3 ± 0.8).


Histological injury of the intestine is less pronounced following PV occlusion, most likely due to higher oxygen and substrate availability during I/R by PV occlusion. This conclusion is supported by a more pronounced metabolic synthetic response (increased glycolysis and fatty acid and amino acid accumulation) with PV occlusion, while oxidative stress was higher with MA occlusion. The inflammatory response showed little difference between the groups.


Intestinal ischemia/reperfusion injury Mesenteric artery occlusion Portal vein occlusion Metabolomics Heat shock proteins