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Purpose: The significance and management of pediatric pneumatosis intestinalis (PI) remains poorly defined. We sought to add clarity in children beyond the neonatal period. Methods: Pediatric patients 3 months–18 years admitted to a quaternary children's hospital with a diagnosis of PI were included in this retrospective study. Pathologic PI was defined as irreversible, transmural intestinal ischemia. Results: 167 children were identified with PI. Of these children, 155 (92.8%) had benign PI and 12 (7.2%) developed pathologic PI. The most common underlying diagnosis for pathologic PI was global developmental delay (75%), although we identified a spectrum of underlying diagnoses at risk for PI. Physical exam notable for abdominal distension (p = 0.023) or guarding (p = 0.028), and imaging with portal venous gas (p < 0.001) or bowel distension (p = 0.001) were significantly associated with pathologic PI. Only 6.6% of all children underwent an operation. For those undergoing non-surgical management of benign PI, 75% of children received antibiotics and average duration of bowel rest was 6.8 days. Conclusions: PI in children is primarily a benign phenomenon and often does not warrant surgical intervention. Bowel rest and antibiotics are therapeutic strategies frequently used in the treatment of this finding. [ABSTRACT FROM AUTHOR]

Aim of the study: Midgut volvulus is a potentially life-threatening condition which is based on intestinal ischemia and reperfusion (I/R) injury. Remote ischemia conditioning (RIC) applied to a limb can protect distant organs such as heart and kidney. The aims of this study were to investigate the effect of RIC on a model of midgut volvulus and to explore its underlying mechanism of action. Methods: Six-weeks old C57BL/6 mice were studied: (a) sham (n = 4): laparotomy alone. (b) Intestinal I/R injury (n = 5): occlusion of the superior mesenteric artery (SMA) for 45 min followed by reperfusion. (c) Intestinal I/R (as in group above) with RIC immediately after reperfusion (n = 5). RIC consisted of 4 cycles of 5 min hind limb ischemia followed by 5 min reperfusion. 24-h after laparotomy, animals were euthanized, and the small intestine (same distance from cecum) was harvested. The intestine was examined for inflammatory cytokines (TNF-α and IL-6), epithelial proliferation marker Ki67 and stem cell marker Lgr5 expression. Main results: Compared to sham, the small intestine of IR mice had more intestinal damage, increased expression of inflammatory cytokines, decreased intestinal proliferation and stem cell activity. RIC significantly counteracted all these changes. Conclusions: Remote ischemia conditioning avoids intestinal damage due to I/R injury. This beneficial effect is associated with decreased intestinal inflammation and enhanced intestinal regeneration. This study implicates that RIC is a novel non-invasive intervention to reduce the intestinal damage occurring in midgut volvulus. [ABSTRACT FROM AUTHOR]

Purpose: Midgut volvulus is associated with intestinal ischemia/reperfusion (IR) injury and can progress to severe intestinal damage. Remote ischemic conditioning (RIC) reduces IR-induced injury in distant organs. The aim of this study was to investigate whether RIC protects the intestine from IR injury. Methods: We investigated intestinal IR injury in 3 weeks old SD rats. Animals underwent: (i) sham laparotomy, (ii) intestinal IR injury, (iii) intestinal IR + RIC during ischemia, or (iv) intestinal IR + RIC after reperfusion. Intestinal IR injury was achieved by 45 min occlusion of superior mesenteric artery followed by de-occlusion. RIC was administered via four cycles of 5 min of hind limb ischemia followed by 5 min reperfusion. Animals were sacrificed 24 h after surgery and the ileum was harvested for evaluation. Results: Intestinal injury was present after IR. However, this injury was reduced in both IR + RIC groups. Expression of inflammatory cytokine IL6 was lower in IR + RIC groups compared to IR alone. Carbonyl protein was also significantly lower in IR + RIC compared to IR, indicating lower oxidative stress in both IR + RIC groups. Conclusion: Remote ischemic conditioning attenuated intestinal injury, inflammation, and oxidative stress in experimental intestinal ischemia/reperfusion injury. Remote ischemic conditioning may be useful in children with midgut volvulus to reduce the intestinal injury. Level of evidence: Experimental study. Type of study: Animal experiment. [ABSTRACT FROM AUTHOR]

Purpose: The roles of commensal bacteria after intestinal ischemia and reperfusion (IIR) are unclear. In current study, we aim to investigate the effects and underlying mechanisms of commensal bacteria in injury and epithelial restitution after IIR.Methods: Commensal gut bacteria were deleted by broad-spectrum antibiotics in mice. IIR was induced by clamping superior mesenteric artery. Intestinal injury, permeability, epithelial proliferation, and proinflammatory activity of mesenteric lymph were investigated.Results: Commensals deletion improved mice survival in the early phase, but failed to improve the overall survival at 96 h after IIR. Commensals deletion reduced proliferation of intestinal epithelial cells (IEC) and augmented proinflammatory activity of mesenteric lymph after IIR. Lipopolysaccharides (LPS) supplement promoted IEC proliferation and improved survival in mice with commensals deletion after IIR. LPS induced production of prostaglandin E2 (PGE2) in mucosa via toll-like receptor 4-NFκB-cyclooxygenase 2 pathway. PGE2 enhanced IEC proliferation in vivo, which was preceded by activation of Akt and extracellular signal-regulated kinase (ERK) 1/2. Blocking of EGFR, PI3K/Akt activity abolished LPS-induced IEC proliferation.Conclusions: Commensal bacteria are essential for epithelial restitution after IIR, which enhance IEC proliferation via induction of PGE2. [ABSTRACT FROM AUTHOR]

Aim of the study: Notch signaling plays important roles in maintaining intestinal epithelial homeostasis. When Notch signaling is blocked, proliferation ceases and epithelial cells become secretory. The purpose of the present study was to evaluate the role of Notch signaling pathway following intestinal ischemia–reperfusion (IR) injury in a rat model. Materials and methods: Male Sprague–Dawley rats were randomly divided into four experimental groups: Sham-24 and Sham-48 rats underwent laparotomy and were killed 24 or 48 h later, respectively; IR-24 and IR-48 rats underwent occlusion of SMA and portal vein for 30 min followed by 24 or 48 h of reperfusion, respectively. Enterocyte proliferation and enterocyte apoptosis were determined at killing. Notch-related gene and protein expression were determined using Real Time PCR, Western blotting and immunohistochemistry 48 h followed IR. Main results: IR-48 rats demonstrated significantly increased rates of cell proliferation and increased cell apoptosis in both jejunum and ileum compared to Sham rats. IR-48 rats exhibited a significant decrease in Notch-1 protein expression (Western blot) that was coincided with a significant decrease in the number of Notch-1 positive cells (immunohistochemistry) in jejunum (35% decrease, p < 0.05) and ileum (twofold decrease, p < 0.05) as well as Hes-1 positive cells in jejunum (28% decrease, p < 0.05) and ileum (31% decrease, p < 0.05) compared to Sham-48 rats. Conclusions: Forty-eight hours following intestinal IR in rats, accelerated cell turnover was associated by inhibited Notch signaling pathway. Intestinal stem cells differentiation toward secretory progenitors rather than differentiation toward absorptive cells is important at this phase of intestinal recovery. [ABSTRACT FROM AUTHOR]

A neonate with gastroschisis had silo placement and near-infrared spectroscopy (NIRS) monitoring of intestinal haemoglobin oxygen saturation (RSO). An ischemic loop of bowel demonstrated decreased RSO, with reversal of clinical ischemia and RSO postoperatively. This demonstrates possible advantage of monitoring intestinal RSO in neonates at risk of ischemia, and response to intervention. [ABSTRACT FROM AUTHOR]

Purpose: A number of patients operated on for Hirschsprung disease continue to have constipation and abdominal distension for years after surgery. Some authors have proposed that ischemia during surgery may induce secondary aganglionosis. The aim of the present study was to study the effects of ischemia on the enteric nervous system of sigmoid colon in an animal model. Methods: A surgical model of colonic ischemia was created. 34 adult Sprague-Dawley rats underwent a laparotomy where the marginal arterioles of the sigmoid colon were ligated. After that, a section in the middle segment of the sigmoid colon was performed followed by an anastomosis. The presence of ischemia was assessed by measurement of visible light spectroscopy tissue oximetry and histological examination. Colonic function was assessed by evaluation of stool weight. Rats were killed at 1, 8 and 12 weeks after the operation. 12 rats were sham-operated. Enteric nervous system was evaluated by means of immunohistochemistry with NGFR p75. Quantitative analysis of the number of ganglia and ganglion cells in the myenteric plexus was performed. Results: The surgical model of colonic ischemia significantly decreased tissue oxygenation (pre-surgical = 54.69 ± 7.32 %; post-surgical = 27.37 ± 9.2 %; p < 0.001). There was no disturbance in body-weight gaining in experimental groups and daily stool output did not vary after surgery (pre-surgical = 4.24 ± 0.94 g; post-surgical = 3.82 ± 1 g; p = 0.09). All experimental groups showed persistent ganglia. However, there was a significant decrease in the number of ganglia in all the experimental groups compared to control (1w: 45.91 ± 7.66; 8w: 44.17 ± 10.56; 12w: 36.17 ± 15.06 vs control: 56.88 ± 8.66; p < 0.01). The number of total ganglion cells was significantly reduced only in the experimental group killed at week 12 compared to control (1w: 539 ± 167.58; 8w: 488.58 ± 154.41; 12w: 343.94 ± 161.91 vs control: 513.96 ± 126.97; p < 0.01). The rate of ganglion cells per ganglia was significantly higher in the groups killed at week 1 and 8 versus control group (1w: 11.63 ± 2.53; 8w: 11.11 ± 2.56; 12w: 9.34 ± 1.16 vs control: 9.02 ± 1.81; p < 0.05). Conclusion: Long-term follow-up after surgically induced colonic ischemia in the rat showed a decreased number of ganglion cells and ganglia. Nevertheless, it did not produce aganglionosis. [ABSTRACT FROM AUTHOR]

Background: Growing evidence suggests that ozone (O) protects the host against pathological conditions mediated by reactive oxygen species by increasing the activity of antioxidant enzymes. The purpose of the present study was to examine the effect of O on intestinal recovery and enterocyte turnover after intestinal ischemia-reperfusion (IR) injury in rats. Methods: Male Sprague-Dawley rats were divided into four experimental groups: (1) sham rats underwent laparotomy; (2) sham-O rats underwent laparotomy and were treated with an ozone/oxygen mixture intraperitoneally and intraluminally (50 %/50 %); (3) IR rats underwent occlusion of both superior mesenteric artery and portal vein for 20 min followed by 48 h of reperfusion, and (4) IR-O rats underwent IR and were treated with an ozone/oxygen mixture similar to group 2. Intestinal structural changes, Park's injury score, enterocyte proliferation and enterocyte apoptosis were determined 48 h following IR. Western blot was used to determine ERK and Bax protein levels. A non-parametric Kruskal-Wallis ANOVA test was used for statistical analysis with p < 0.05 considered statistically significant. Results: Treatment of IR rats with O resulted in a significant increase in mucosal weight in jejunum (70 %) and ileum (32 %), mucosal DNA (twofold increase) and protein (35 %) in ileum, villus height and crypt depth in jejunum (61 and 16 %, correspondingly) and ileum (31 and 43 %, correspondingly) compared to IR animals. IR-O rats also had a significantly lower intestinal injury score as well as a lower apoptotic index in jejunum and ileum compared and IR animals. A significant increase in cell proliferation rates in IR-O animals was accompanied by increased levels of p-ERK protein. Conclusions: Treatment with ozone prevents intestinal mucosal damage, stimulates cell proliferation and inhibits programmed cell death following intestinal IR in a rat. [ABSTRACT FROM AUTHOR]

Objectives: The usefulness of omega-3 lipid emulsions has been extensively studied. The objectives of the present study were to examine the effect of an omega-3 lipid emulsion in reducing oxidative stress in a rat model of intestinal ischemia−reperfusion injury and the underlying mechanism. Methods: A total of 66 rats were divided into three dietary groups (lipid-free, soybean oil, and fish oil groups). Each animal was administered total parenteral nutrition for 3 days, followed by induction of intestinal ischemia for 100 min. Animals subjected to sham surgery served as the controls. Intestinal tissue and blood were harvested 6 and 12 h after the surgery, then, assessment of the histological damage score, plasma-related parameters, and statistical evaluation were performed. Results: The histological damage score in the intestinal tissues was significantly lower in the fish oil group than in the soybean oil group ( P = 0.0121). The late-phase urinary level of 8-hydroxy-2-deoxyguanosine was also significantly lower in the fish oil group as compared with that in the other groups ( P = 0.0267). Furthermore, the plasma level of high-mobility group box 1 protein was also significantly lower in the fish oil group as compared with that in the lipid-free group ( P = 0.0398). Conclusion: It appeared that intravenous administration of an omega-3 lipid emulsion prior to ischemia−reperfusion injury reduced the oxidative stress and severity of tissue damage. Modification of membrane fatty acids may serve as the mechanism underlying this reduction of tissue damage. [ABSTRACT FROM AUTHOR]

We report a newborn who presented with acute abdominal distension secondary to gastric ischaemia with an associated undiagnosed coarctation of the descending aorta. This is the first description of such a previously unrecognised association, which is discussed further with reference to the current literature. [ABSTRACT FROM AUTHOR]

In infants with necrotizing enterocolitis (NEC), intestinal gangrene defines advanced disease. Since intestinal ischemia is considered a pathogenetic factor for intestinal gangrene, serum activity of mucosal and seromuscular enzymes may be elevated in these patients. Our aim was to evaluate if serum enzymes activity is increased in infants with NEC associated with intestinal gangrene. We performed a retrospective review of the case notes of infants operated on for NEC between 1998 and 2006. Patients with preoperative determination of serum enzymes were included in the study, and were divided into Group A and Group B based on the presence or absence of intestinal gangrene, respectively. Serum activities of alkaline phosphatase (ALP), glutamic oxaloacetic transaminase (GOT), creatine kinase (CK), and lactate dehydrogenase (LDH) were compared in the two Groups. Values are medians (interquartile range). Thirty-five infants were operated on for NEC in the study period. Eighteen patients fulfilled the inclusion criteria: 12 in Group A and six in Group B. Group A patients had significantly higher LDH activity [1131.0 (1092.0-1300.0) vs. 482.0 (440.0-624.5) IU/L; P < 0.005]. Our findings suggest that LDH activity may be increased in infants with NEC and intestinal gangrene. Its evaluation could be a further tool in the surgical decision making process in infants with NEC. [ABSTRACT FROM AUTHOR]

Intestinal malrotation (IM) and cardiovascular defects (CCVD) are both common congenital defects. We investigated the prevalence and types of CCVD in a 25-year IM population, and its association with post-IM-operative morbidity and mortality. Data on the type of CCVD, other congenital defects, syndromes, associations, post-IM-operative morbidity and mortality were retrospectively reviewed from the records of IM patients born between 1980 and 2005. Data were analyzed on (significant) differences between CCVD subgroups, and risk factors for both morbidity and mortality were calculated. Seventy-seven of 284 IM patients (27.1%) were diagnosed with a major or minor CCVD (37 and 40 patients, respectively). Syndromes and associations were more frequently diagnosed in patients with major than with a minor CCVD (67.6 vs. 40%, respectively). Post-IM-operative complications, although frequently observed (61%), did not differ between patients with major and minor CCVD. Physical CCVD signs before IM surgery increased post-IM-operative morbidity significantly (OR 4.0, 95% CI 1.4-11.0). Fifteen patients died (19.5%), seven due to cardiovascular cause. Mortality risk was increased by intestinal ischemia and post-IM-operative complications and by major CCVD after correction for age at weight at the time of IM operation. Congenital cardiovascular defects in children with intestinal malrotation are common, with high morbidity and mortality rates after IM operation. Elective IM surgery in young patients with CCVD should be performed in a centre with adequate paediatric cardiac care. Benefits of laparoscopic intervention need further study. [ABSTRACT FROM AUTHOR]

Recent evidence suggests that neutrophil recruitment may initiate cell apoptosis in ischemic tissues. We have recently shown that enterocyte apoptosis is increased following intestinal ischemia-reperfusion (IR) injury. The purpose of the present study was to examine the effect of hyperoxia on E-selectin expression, neutrophil recruitment and enterocyte apoptosis following intestinal IR in a rat. Male Sprague-Dawley rats were divided into three experimental groups: (1) sham rats underwent laparotomy without vascular occlusion and were ventilated with air (Sham) (2) IR rats underwent occlusion of both the superior mesenteric artery and portal vein for 30 min and were ventilated with air (IR), and (3) IR-O2 rats underwent IR and were ventilated with 100% started 10 min before reperfusion and continued for 6 h (IR-O2). Intestinal structural changes were determined 24 h following IR. Immunohistochemistry for E-selectin (using E-selectin cleaved concentrated polyclonal antibody) was performed to identify E-selectin immunoreactivity localized to the endothelium of venules. The recruitment of neutrophils was calculated per 100 venules. Immunohistochemistry for Caspase-3 was performed for identification of apoptotic cells. Non-parametric one-way ANOVA test was used for statistical analysis with p less than 0.05 considered statistically significant. A significant increase in E-selectin expression in the jejunum (6.1 ± 2.2 vs. 2.5 ± 1.0 E-selectin positive vessels/100 vessels, p < 0.05) and ileum (12.1 ± 2.7 vs. 3.3 ± 1.2 E-selectin positive vessels/100 vessels, p < 0.05) and a concomitant increase in neutrophil recruitment in the ileum (5.5 ± 1.6 vs. 1.3 ± 0.6 adhered PMN’s per 100 venules) were observed in IR rats compared to sham animals and were accompanied by increased cell apoptosis ( p < 0.05). Treatment with 100% oxygen resulted in a significant attenuation in E-selectin expression in the ileum (2.7 ± 1.1 vs. 12.1 ± 2.7 E-selectin positive vessels/100 vessels, p < 0.05), and neutrophil recruitment in the jejunum (2.5 ± 1.4 vs. 7.7 ± 1.9 adhered PMN’s per 100 venules, p < 0.05) and ileum (1.5 ± 0.7 vs. 5.5 ± 1.6 adhered PMN’s per 100 venules, p < 0.05) compared to IR animals, and was accompanied by decreased cell apoptosis ( p < 0.05). Hyperoxia inhibits enterocyte apoptosis following intestinal ischemia-reperfusion. Down-regulation of E-selectin expression with subsequent decrease in neutrophil recruitment may be responsible for this effect. [ABSTRACT FROM AUTHOR]

Many biochemical markers have been investigated in intestinal ischemia. However, the effects of intestinal ischemia on the level of serum immunoglobulin A (IgA) has apparently not been investigated in the literature, although the gastrointestinal system is one of the main sources of serum IgA. The aim of our study was to evaluate the changes of serum IgA levels during intestinal ischemia of varying duration in rats. Group 1 (n=5) was created for control purposes, including the detection of the baseline values and the effects of the anesthetic agents. Group 2 (n=20) rats underwent sham laparotomy. Group 3 (n=20) had 50% of small intestine ischemia by the strangulated obstruction model. Serum samples were obtained by cardiac puncture 1 h after anesthetic agents were given in group 1. On the other hand, serum and intestine samples were obtained at 1 (T1, n=5), 2 (T2, n=5), 4 (T4, n=5) and 6 (T6, n=5) h after the operation in groups 2 and 3. The levels of serum IgA, lactic dehydrogenase (LDH) and alkaline phosphatase (ALP) were determined. Pathologic specimens were graded in a masked manner. IgA levels were abruptly decreased to 8.49±1.58 mg/dl in rats with intestinal ischemia at 1 h after the operation. This decrease in serum IgA at T1 in group 3 was statistically significant compared with the control and sham-operated groups (18.80±1.15 mg/dl, 22.07±1.54 mg/dl, respectively; P<0.01). On the other hand, IgA levels were significantly elevated at T2 in the sham-operated group compared with control and intestinal ischemia groups (26.99±2.96 mg/dl, 18.80±1.15 mg/dl, 14.35±2.62 mg/dl, respectively; P<0.05). The serum IgA levels decreased to above baseline values at T6 in group 2 (19.60±2.78 mg/dl), while they increased to below baseline values in group 3 (17.60±1.28 mg/dl). In group 3, IgA levels were elevated to baseline values, while a significant ischemia occurred at 4 and 6 h after operation. These results suggested that serum IgA is affected earlier by intestinal ischemia and intestinal manipulation. The increase in serum IgA levels may be related to stimulation of the local immune responses in the intestine. On the other hand, abruptly decreasing serum IgA levels in this experimental study may be related to inadequate transport of the synthesized IgA to the systemic circulation, because serum IgA levels were returned to baseline values while a significant ischemia occurred at T4 and T6. According to these results, we conclude that serum and peritoneal fluid IgA levels may be changed by intestinal ischemia and may be used to make an early diagnosis of intestinal ischemia in humans. [ABSTRACT FROM AUTHOR]

Major consequences of ischemic bowel disorders are: enhanced transcapillary filtration, interstitial edema, and sequestration of fluid in the lumen of the bowel. Although several endogenous substances (histamine, prostaglandine, etc.) are released from the small bowel, specific inhibitors do not prevent increased intestinal vascular premeability produced by ischemia reperfusion. Cytotoxic oxygen metabolites - so-called oxygen free radicals - are generated in excess after ischemia during the early reperfusion period and endogenous defense mechanisms are overwhelmed. The highly reactive oxygen radicals damage proteins, lipids, carbohydrates, and nucleotides. Experimental studies showed that pretreatment with oxygen free radical scavengers (super-oxide dismutase, catalase, dimethylsulfoxide) provided significant protection againts ischemic injuries to the small bowel. Further studies gave evidence that the enzyme xanthine oxidase, which reacts with hypoxanthine, constitutes the primary source of oxygen radical production after intestinal ischemia. Xanthine oxidase inhibitors (allopurinol, pterin aldehyde) are powerful substances attenuating the ischemia-induced increase in intestinal vascular permeability. Morphometric studies on biopsies obtained after reperfusion of the intestine indicated likewise that pretreatment with superoxide dismutase, allopurinol, etc. largely prevented the typical intestinal epithelial necrosis induced by ischemia reperfusion. The experimental results are promising for further clinical research. It is conceivable that drugs such as allopurinol or superoxide dismutase may become useful as a treatment of ischemic gastrointestinal diseases, such as necrotizing enterocolitis, volvulus, and others. [ABSTRACT FROM AUTHOR]

Intestinal ischemia was created after a limited laparotomy by ligation of the terminal mesenteric vessels in the last 10 cm of distal ileum in 2-day-old piglets. Five groups (each n = 15) were studied: 1 (unoperated control group, killed on day 4), 2 (sham control with laparotomy, killed on day 4), 3 (ischemia, killed on day 4), 4 (ischemia, killed on day 9), and 5 (unoperated control on day 9, not killed). All animals in groups 1, 2 and 5 survived. Two animals in group 3 and 1 in group 4 died (peritonitis and distal ileal perforation). In animals killed on day 9, less weight gain was observed in group 4 compared to the unoperated controls. Macroscopically, no alteration was found at laparotomy in the animals in group 1, whereas in group 2, 1 animal showed beginning peritonitis and another some degree of peritoneal adhesions in group 3, 1 piglet had an intestinal perforation and 4 had intestinal distention above the ischemic loop. In group 4, 7 animals had dilatation of the upper loops, 4 a complete stricture, and 3 peritonitis with complete necrosis of the distal ileum. Microscopic examination revealed severe lesions of the ischemic area in groups 3 and 4 and mild lesions of the upper loop. The kidney was contaminated by translocation of gram-positive cocci in 36% of cases in group 2. Germ carriage for staphylococci was estimated at 80% in the terminal ileum of animals in group 3 versus 8.3% in group 2. In groups 3 and 4, the translocation rate was 30% in the kidney and 40% in the liver. Low disaccharidase activities were found in ischemic areas in groups 3 and 4, with no difference in activity in the upper loops. [ABSTRACT FROM AUTHOR]

The intestinal lesions caused by ischemia and reperfusion may lead to grave sequelae. To study the efficacy of adenosine triphosphate magnesium chloride (ATP-MgCl) and allopurinol (ALLO) in protecting the small bowel from ischemia, rabbits in two groups, 1 ( n = 7) and 2 ( n = 7), were pretreated with either 1 ml saline or ATP-MgCl just prior to intestinal ischemia and reperfusion. Group 3 ( n = 7) animals recieved enteral ALLO daily for 3 days before the experiment. Using Oldham and Thompson's grading system, histologic specimens were evaluated blindly for evidence of ischemic-reperfusion injury. The histologic injury scores in group 2 were significantly lower than those in groups 1 and 3 ( P <0.05 and 0.02, respectively) after 2 h of ischemia. Following 30 min of reperfusion, histologic injury scores rose significantly in group 1 ( P <0.05), decreased in group 2 ( P <0.005), and showed no significant changes in group 3 ( P >0.50). We conclude that: (1) pretreatment with ALLO can prevent reperfusion injury of the small intestine; and (2) ATP-MgCl administration can reduce 2-h ischemic intestinal damage, reverse reperfusion-induced cellular injury, and improve the recovery of ischemic bowel during the reperfusion phase. [ABSTRACT FROM AUTHOR]