Pathophysiology of mesenteric ischemia/reperfusion: a review

Abstract

During ischemia, the cell structures are progressively damaged, but restoration of the blood flow, paradoxically, intensifies the lesions caused by the ischemia. The mechanisms of ischemia injury and reperfusion (I/R) have not been completely defined and many studies have been realized in an attempt to find an ideal therapy for mesenteric I/R. The occlusion and reperfusion of the splanchnic arteries provokes local and systemic alterations principally derived from the release of cytotoxic substances and the interaction between neutrophils and endothelial cells. Substances involved in the process are discussed in the present review, like oxygen-derived free radicals, nitric oxide, transcription factors, complement system, serotonin and pancreatic proteases. The mechanisms of apoptosis, alterations in other organs, therapeutic and evaluation methods are also discussed.

Neutrophil priming by hypoxic preconditioning protects against epithelial barrier damage and enteric bacterial translocation in intestinal ischemia/reperfusion

“…The pelleted cells were mixed with red blood cell lysis buffer (150 mM NH 4 Cl and 20 mM NaHCO 3 in water) and incubated for 6 min on ice until the turbidity was lost and the solution became clear. The cells were washed, resuspended with 200 ml of PBS and analyzed by FACS.…”

“…The tube was put on ice for 30 min and the supernatant was collected for centrifugation at 270 Â g for 10 min at 4 1C. The contaminating erythrocytes in the pellet were lysed with 0.83% (w/v) NH 4 Cl in water for 5 min and then the solution was centrifuged at 480 Â g for 10 min at 4 1C. The pelletcontaining neutrophils was washed with Hank's buffered saline solution (HBSS) at 270 Â g for 8 min at 4 1C, resuspended in HBSS and the cell number determined using a hemocytometer.…”

“…[1][2][3] Intestinal I/R may trigger mucosal barrier damage and enteric bacterial translocation (BT), leading to development of septic complications. 4,5 The intestine contains over 100 trillion commensal bacteria that are normally restricted to the lumen. 6,7 Germ-free rodents subjected to mesenteric I/R exhibited less intestinal and lung histopathology, and showed higher survival rates than conventionally raised animals, underscoring the role of enteric bacteria in the pathogenesis of I/R-induced local and remote organ dysfunction.…”

R-spondin3 prevents mesenteric ischemia/reperfusion-induced tissue damage by tightening endothelium and preventing vascular leakage

“…Mesenteric ischemia (ischemia of the small intestine) is a common life-threatening abdominal emergency encountered in a variety of clinical and surgical settings (1)(2)(3). Acute mesenteric ischemia induces local cellular changes such as cytoskeletal disorganization, up-regulation of adhesion molecules, and neoantigen expression that provokes an intense inflammatory response and endothelial barrier dysfunction during subsequent reperfusion.…”

Effects of allopurinol and preconditioning on apoptosis due to ischemia-reperfusion on a double jejunum-segment canine model

“…Chiu et al 3 evaluated the ischemia-reperfusion intestinal injury and classified this process in characteristic histological grades. Similarly to other organs, free radicals play an important role in the pathophysiology of mesenterial I/R injury [4][5][6] , leading to different type of cell death, such as apoptosis or necrosis 7,8 .…”