Intestinal ischemia/reperfusion (I/R) injury occurs frequently in a variety of clinical settings, including mesenteric artery occlusion, abdominal aneurism surgery, trauma, shock, and small intestinal transplantation, and is associated with substantial morbidity and mortality. Although the exact mechanisms involved in the pathogenesis of intestinal I/R injury have not been fully elucidated, it is generally believed that polymorphonuclear neutrophils, pro-inflammatory cytokines, and mediators generated in the setting of oxidative stress, such as reactive oxygen species (ROS), play important roles. Heme oxygenase (HO) is the rate-limiting enzyme that catalyzes the degradation of heme into equimolar quantities of biliverdin and carbon monoxide (CO), while the central iron is released. An inducible form of HO (HO-1), biliverdin, and CO, have been shown to possess generalized endogenous anti-inflammatory activities and provide protection against intestinal I/R injury. Further, recent observations have demonstrated that exogenous HO-1 expression, as well as exogenously administered CO and biliverdin, have potent cytoprotective effects on intestinal I/R injury as well. Here, we summarize the currently available data regarding the role of the HO system in the prevention intestinal I/R injury.

/pdf/application-of-heme-oxygenase-1-carbon-monoxide-and-4oohgd1yft.pdf

Application of Heme Oxygenase-1, Carbon Monoxide and Biliverdin for the Prevention of Intestinal Ischemia/Reperfusion Injury

Background Apoptosis has been identified after ischemia-reperfusion (IR) injury to the brain, heart, kidney, retina, and the adrenals. Intestinal IR injury causes villous and crypt damage, which has so far been attributed to cellular necrosis. This study was undertaken to investigate the possible role of apoptosis after reperfusion of cold-stored small bowel grafts in syngeneic rats. Methods Small intestinal grafts were stored at 4 degrees C for 24 hr in saline (n=6) or in modified University of Wisconsin solution (n=6), followed by reperfusion for 1 hr in syngeneic Lewis rats. Small bowel samples were obtained before storage, after preservation and after 1 hr of reperfusion. They were processed for light and electron microscopy and analyzed for cell death, with particular emphasis on apoptosis. Results Less than one apoptotic event was seen per 10 crypts in normal and stored bowels. An occasional normal and some denuded villous epithelial cells of stored bowels exhibited apoptosis. After isotransplantation and 1 hr of reperfusion, marked increase in apoptosis was seen in the crypts and denuded villous epithelial cells of both saline- and modified University of Wisconsin-stored bowels. Secondary necrosis was seen in apoptotic cells, as were dark cells. Only a few cells showed signs of primary ischemic necrosis. Conclusions Apoptosis occurs after intestinal IR injury. Modulation of its genetic regulatory and biochemical effector machinery might alleviate or even prevent IR injury in small bowel transplanted after similar periods of storage.

Apoptosis after intestinal ischemia-reperfusion injury: a morphological study.

https://onlinelibrary.wiley.com/doi/pdf/10.1034/j.1600-6143.2002.20307.x

Defining the Role of a Tailored Luminal Solution for Small Bowel Preservation

Intestinal ischaemia-reperfusion (IR) injury has largely been attributed to cellular necrosis. Apoptosis, a distinct form of cell death has been observed following IR to the brain, heart, adrenals and the kidneys. In order to characterize the role of apoptosis in intestinal IR, small bowel grafts were stored in saline (n = 6) or modified University of Wisconsin solution (n = 6) at 4 degrees C for 12 h and reperfused for 6 h in syngeneic rats. Samples of normal, stored and reperfused intestines at 1, 3 and 6 h were analysed by light and electron microscopy. Following reperfusion, there was crypt and villous epithelial apoptosis, loss of crypt and villous structures, and an increase in mucosal inflammatory cell infiltration. Ongoing apoptosis was maximum at 1 h, its degree decreasing with increasing reperfusion intervals. Large numbers of apoptotic bodies dominated the picture from 3 h of reperfusion. This study has demonstrated the induction of apoptosis by intestinal IR injury, which begins within an hour of reperfusion and is probably responsible for the observed crypt and villous loss. This has potential therapeutic implications as, opposed to necrosis, apoptosis is an active process with genetic regulators and biochemical effectors, which can be specifically targeted to prevent or alleviate IR injury.

Characterization of apoptosis in intestinal ischaemia-reperfusion injury — a light and electron microscopic study.

A newly developed solution enhances thirty-hour preservation in a canine lung transplantation model.

Effect of luminal flush on mucosal injury during cold ischemia in the rat small bowel

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Effect of luminal flush on mucosal injury during cold ischemia in the rat small bowel