Reperfusion injury in the equine intestine

Rowe, Emma L.; White, Nathaniel A.

doi:10.1053/ctep.2002.35578

Cited by 14 publications

(21 citation statements)

References 83 publications

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“…In clinical cases of small intestinal strangulation, remaining viable margins display inflammatory changes marked by neutrophil infiltration in the seromuscular layer and mucosa/submucosa (Gerard et al 1999), consistent with changes that characterize reperfusion injury (Rowe and White 2002). Neutrophilic inflammation in equine jejunal myenteric layers 18 hours after intraoperative manipulation to decompress small intestine coincides with the time point at which POI typically develops (Little et al 2005).…”

Section: Methods For Inducing Ischemiamentioning

confidence: 67%

“…Ischemia disrupts aerobic cellular metabolism, which decreases intracellular ATP and pH , Rowe and White 2002, McMichael and Moore 2004, inactivates transmembrane ion pumps, causes an intracellular accumulation of Ca 2+ , Na + , and lactate, and disrupts intracellular organelles, cytoskeletal elements and tight junctions , Carden and Granger 2000, Li et al 2009, Ivanov et al 2010. The biochemical steps responsible for I/R are initiated by oxidation of hypoxanthine to xanthine (X) by xanthine oxidase (XO), both of which are generated during the ischemic period.…”

Section: Ischemic Injurymentioning

confidence: 99%

“…Equine small and large intestines behave differently in response to reperfusion (Kooreman et al 1998, Dabareiner et al 2001, Rowe and White 2002. There is some evidence that reperfusion injury can occur in the equine small intestine (Dabareiner et al 1995/2001, with low-flow ischemic models providing the most compelling evidence of postischemic damage (Van Hoogmoed et al 2001, Rowe and.…”

Section: Reperfusionmentioning

confidence: 99%

“…Thus, alternative oxidants, mitochondrial dysfunction, failure of mucosal postcapillary microcirculation, collateral tissue damage by infiltrating neutrophils, uncontrolled activation of an innate immune response, or simply a time-related continuation of injury initiated during ischemia, might be responsible for colonic mucosal damage after reperfusion , Wilkins et al 1994, Granger and Korthuis 1995, Blikslager et al 1997, McAnulty et al 1997, Rowe and White 2002.…”

Section: Reperfusionmentioning

confidence: 99%

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Ischemia in equine intestine – mechanisms of injury and methods of treatment

Freeman¹,

Grosche²

2012

PHK

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SummaryThe importance of reperfusion injury in equine intestine is controversial and unclear. Large colon volvulus and small intestinal strangulation are the most devastating causes of intestinal ischemia in horses and result in severe mucosal damage, barrier dysfunction, endotoxic shock and death. Although essential for tissue recovery, reperfusion after these types of ischemia could exacerbate intestinal injury. Responses to ischemia and reperfusion (I/R) involve a series of synchronized biochemical, cellular and structural changes characterized by generation of reactive oxygen metabolites, activation of immune cells, and epithelial cell degeneration and death. The intensity of neutrophil activation and influx is central to the process of reperfusion injury and the associated inflammatory events. The classic paradigm of reperfusion injury is best displayed after the segmental hypoperfusion or low-flow ischemia model, in which arterial inflow is adjusted to 20% of normal baseline flow, and then allowed to return to normal or greater values during reperfusion. In such cases, injury during the ischemic phase is mild, compared with the reperfusion injury that follows. Although there is some evidence of reperfusion injury in equine colon and jejunum after low-flow ischemia, attempts to ameliorate this by pharmacologic means have met with only moderate success. A multimodal approach, using solutions designed to improve survival in transplanted organs, seems to hold the greatest promise, although these have not been embraced in the clinical setting. Expense and difficulties in delivery are the two most serious limitations. Recent studies to assess the effect of colonic I/R on equine pelvic flexure involved a complete ischemia model that was similar to the clinical lesion, and for periods of 1 to 2 hours of ischemia followed by 30 minutes, 4 hours, or 18 hours of reperfusion. Ischemia caused degeneration and detachment of epithelial cells, early apoptosis, and opening of tight junctions (TJs), all of which decreased transepithelial resistance (TER) and increased mannitol flux when the tissues were studied in vitro. Autophagy was a prominent feature in epithelial cells after 1 hour of ischemia. Reperfusion was characterized by apoptosis, epithelial regeneration, and closure of TJs with improved TER and reduced mannitol leakage. Neutrophils infiltrated colonic mucosa during reperfusion, and macrophages, mast cells and eosinophils were activated during I/R. Equine colonic mucosa subjected to ischemia can repair rapidly and regain barrier integrity during reperfusion, despite intense mucosal inflammation. Recently, attention has focused on inflammation induced by intestinal handling and on remote organ responses to intestinal injury, both of which could be highly relevent to postoperative management of horses that undergo colic surgery. The use of lidocaine in a continuous rate infusion is a popular approach to ameliorate the intestinal inflammatory response after colic surgery, although there is no evidence that it has a...

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Section: Methods For Inducing Ischemiamentioning

confidence: 67%

Section: Ischemic Injurymentioning

confidence: 99%

Section: Reperfusionmentioning

confidence: 99%

Section: Reperfusionmentioning

confidence: 99%

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Ischemia in equine intestine – mechanisms of injury and methods of treatment

Freeman¹,

Grosche²

2012

PHK

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“…Intestinal ischemia may be classified into acute mesenteric ischemia, chronic mesenteric ischemia, and ischemic colitis which culminate in decreased blood supply to tissues and reduced intestinal oxygen (Rowe & White 2002, Yasuhara 2005, Kaszaki et al 2006.…”

Section: Introductionmentioning

confidence: 99%

Allogenic mesenchymal stem cell intravenous infusion in reparation of mild intestinal ischemia/reperfusion injury in New Zealand rabbits

et al. 2018

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The present study aimed to evaluate the efficacy of mesenchymal stem cell (MSC) infusion, derived from adipose tissue, on reduction of local and remote tissue damage caused by the event of experimental intestinal I/R in New Zealand breed rabbits. For obtaining, characterization, and cultivation of MSC derived from adipose tissue (MSC-Adp), 3 juvenile animals (four months old) were used. The cells were considered to be viable for therapy after the fourth passage (in vitro phase). For the in vivo stage, 24 young adult animals (six months old) were used, weighing approximately 3.5 kg, in which were randomly divided into two groups, called: IR treated with MSC (I2H/R5H MSC 3D; I2H/R5H MSC 7D); IR treated with PBS (I2H/R5H PBS 3D; I2H/R5H PBS 7D). The animals were anesthetized and submitted to pre-retro-umbilical midline celiotomy. The extramural peri-intestinal marginal artery was located and clamped (predetermined and standardized region) with the aid of a vascular clip, promoting a 2 hour blood flow interruption. After this period, blood flow was reestablished, inhalatory anesthesia was suspended, and the animals awaken. After 5 hours of reperfusion, the treatments were performed by intravenous infusion according to the experimental groups. The animals were evaluated 72 hours and seven days after the treatment as for the macroscopic appearance (color and peristaltism) of the jejunal segment, and by histological evaluation of the ischemic segment for the presence or absence of destruction of the intestinal mucosa, edema, bleeding, dilation of lymph vessels, and presence of polymorphonuclear inflammatory cells, both in the mucosa and submucosa. The observed results revealed that the groups treated with MSC-Adp obtained smaller mucosal and submucosal lesions when compared to the groups treated with PBS. Also, MSC-Adp treated groups obtained controlled inflammatory response and higher mitotic rate, outcomes related to the therapeutic potential of MSC. Infusion of stem cells attenuated the lesions caused by intestinal I/R in both MSC groups when compared to the group treated with PBS.

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