Superior Mesenteric Artery Ischemia Research Articles

Surgical strategies and efficacy analysis for aortic dissection complicating intractable mesenteric artery ischemia

Objective: To explore the surgical strategies and clinical efficacy for aortic dissection combined with refractory superior mesenteric artery (SMA) ischemia. Methods: This is a retrospective case series study. Clinical data of 24 patients with aortic dissection and refractory SMA ischemia admitted to the Department of Vascular Surgery, Zhongshan Hospital, Fudan University from August 2010 to August 2020 were retrospectively collected. Of the 24 patients, 21 were males and 3 were females, with an age of (50.3±9.9) years (range: 44 to 72 years).Among them, 9 cases were Stanford type A aortic dissection, and 15 cases were type B. All patients underwent CT angiography upon admission, and based on imaging characteristics, they were classified into three types. Type Ⅰ: severe stenosis/occlusion of the SMA true lumen only; Type Ⅱ: stenosis of the true lumens in the descending aorta and SMA (isolated type); Type Ⅲ: stenosis of the true lumens in the thoracoabdominal aorta and SMA (continuation type). Surgical procedures, complications, mortality, and reintervention rates were recorded. Results: Among the 24 patients, 17 (70.8%) were classified as Type Ⅰ, 4 (16.7%) as Type Ⅱ, and 3 (12.5%) as Type Ⅲ. Fourteen cases of Type Ⅰ underwent thoracic endovascular aortic repair combined with SMA stent implantation. Additionally, 3 Type Ⅰ and 1 Type Ⅱ patients underwent only SMA reconstruction (with one case of chronic TAAD treated with iliac artery-SMA bypass surgery). Moreover, 3 Type Ⅱ and 3 Type Ⅲ patients underwent descending aorta combined with SMA stent implantation. There were 5 patients (20.8%) who underwent small bowel resection, either in the same sitting or in a staged procedure. During hospitalization, 4 patients died, resulting in a mortality rate of 16.7%. Among these cases, two patients succumbed to severe intestinal ischemia resulting in multiple organ dysfunction syndrome. The follow-up duration was (46±9) months (range: 13 to 72 months). During the follow-up, 2 patients died, unrelated to intestinal ischemia. The 5-year freedom from reintervention survival rate was 86.1%, and the 5-year cumulative survival rate was 82.6%. Conclusions: Patients with aortic dissection and refractory SMA ischemia have a high perioperative mortality. However, implementing appropriate surgical strategies according to different clinical scenarios can reduce mortality and alleviate intestinal ischemia.

Gastrointestinal Bleeds.

Gastrointestinal Bleeds.

A Case of Acute Superior Mesenteric Artery Ischemia with an Atypical Clinical Course Due to the Presence of Collateral Blood Vessels

A Case of Acute Superior Mesenteric Artery Ischemia with an Atypical Clinical Course Due to the Presence of Collateral Blood Vessels

Effects of Receptor for Advanced Glycation End-Products (RAGE) Signaling on Intestinal Ischemic Damage in Mice

Objective: Superior mesenteric artery ischemia and nonocclusive mesenteric ischemia are representative diseases of the vascular emergency known as irreversible transmural intestinal necrosis (ITIN). The receptor for advanced glycation end-products (RAGE) belongs to the immunoglobulin superfamily of extracellular ligands, which also includes high-mobility group box 1 (HMGB-1) and proteins of the S100 family. The HMGB-1 ligands have been implicated in the pathogenesis of various inflammatory disorders. This study was designed to investigate the relation between RAGE and ITIN in a murine acute intestinal ischemic model. Materials and Methods: ITIN was induced by clipping the cranial mesenteric artery and the peripheral blood vessels. Mucosal and blood samples were collected and analyzed by reverse-transcription PCR and immunohistochemistry for mucosal inflammation and levels of RAGE-related proteins. The influence of RAGE signaling on intestinal cell reproduction was investigated using the cell scratch test, an in vitro wound-healing assay. Finally, RAGE-related proteins and their respective inhibitors were administered intraperitoneally to ITIN model mice to determine their effects. Results: RAGE-expressing cells were located at the base of the intestinal crypts at day 0. As ITIN progressed, most of the damaged intestinal cells expressed RAGE, and ligands of RAGE such as HMGB-1, S100 A8/A9, and S100β were present in the crypt cells from the bottom to the top. The quantities of S100 A8/A9 and S100β were particularly high, above the levels found in other diseases. When S100 A8/A9 and S100β were applied to small intestinal epithelial cells in vitro, regeneration was significantly impeded. Inflammatory Gr1+ neutrophils and F4/80+ macrophages are involved in tissue ischemia. S100 A8/A9 enhances inflammatory myeloid cell influx. Conclusions: RAGE-related proteins are elevated in ITIN model mice and impede intestinal regeneration in vitro. RAGE-related proteins may be a new therapeutic target or a new marker for ITIN.

Quantification of Mesenteric Blood Flow by Magnetic Resonance Flow Imaging in Patients with Arterial Dissection.

Mesenteric ischemia is an infrequent, but potentially dangerous, complication of aortic or mesenteric artery dissection. Severe mesenteric ischemia presenting as a malperfusion syndrome, caused by aortic dissection or isolated mesenteric dissection, should be treated immediately by central aortic repair or angioplasty. However, treatment of non-critical, symptomatic mesenteric ischemia without narrowing true lumen of the aorta or localized mesenteric artery dissection was difficult. We treated two distinctly different cases of non-critical, symptomatic mesenteric ischemia superior mesenteric artery ischemia needing intensive care and mesenteric blood flow was determined by quantification with cine-phase contrast magnetic resonance imaging.

Mesenteric Artery Stenosis Presenting as Severe Erosive Gastroduodenitis: A Rare Case Report With Long Term Follow-Up

Superior Mesenteric artery ischemia is a rare condition with serious clinical consequences. It may be caused by either mechanical or non mechanical obstruction of the artery. These patients usually present with recurrent abdominal pain usually occurring after meals. We report a 45 yr old male, who presented with pain abdomen and epigastric burning sensation which increases with food consumption from the past 6 months. Patient was evaluated and was found to have severe erosive Gastroduodenitis which was secondary to superior mesenteric artery stenosis diagnosed on CT Abdomen. Patient underwent successful Superior Mesenteric Artery (SMA) stenting. Repeat upper gastrointestinal endoscopy during follow up after 1 year showed complete resolution of the duodenal mucosa and was asymptomatic. Key words: Superior mesenteric artery stenosis, Duodenal ischemia, Pain abdomen, Stenting.

Endovascular interventional treatment for acute superior mesenteric artery ischemia

Objective To investigate the feasibility and safety of endovascular interventional treatment for acute superior mesenteric artery ischemia. Methods The clinical data of 55 patients with acute superior mesenteric artery ischemia who were admitted to the First Affiliated Hospital of Chongqing Medical University from July 2011 to December 2014 were retrospectively analyzed. The result of preoperative digital subtraction angiography (DSA) was in accord with computed tomography (CT), showing that 34 patients had superior mesenteric artery trunk embolism, 17 patients had superior mesenteric artery branch embolism, and 4 patients had artery dissection complicated with acute thrombosis. All patients firstly received endovascular interventional treatment. Abdominal exploration would be done if abdominal symptoms, signs, blood routine and imaging examinations indicated intestinal necrosis. Enterotomy and enteroanastomosis were done when intestinal necrosis was confirmed during the operation. Patients were followed up by outpatient examination till March 2015. The outcomes of endovascular interventional treatment, sequential treatment after endovascular interventional treatment, postoperative complications, 30-day mortality, recurrence rate and mortality during the follow-up were analyzed. Results The median duration from onset of symptoms to endovascular intervention was 10.1 hours (range, 4.0-15.0 hours). Complete recanalization rate was 32.7%(18/55), including 8 cases of superior mesenteric artery trunk embolism, 9 cases of superior mesenteric artery branch embolism and 1 case of superior mesenteric artery dissection. Partial technical recanalization rate was 63.6%(35/55), including 26 cases of superior mesenteric artery trunk embolism, 8 cases of superior mesenteric artery branch embolism and 1 case of superior mesenteric artery dissection. Two patients who did not respond to endovascular interventional treatment recovered after stent implantation. Nine patients with superior mesenteric artery trunk embolism underwent laparotomy+ enterectomy+ enteroanastomosis within 11-24 hours after thrombolysis. The mean length of resected small intestine was 103 cm (range, 74-201 cm). During hospitalisation, 2 patients suffered from puncture site bleeding and recovered after compression hemostasis and no patient suffered from massive hemorrhage. All the 55 patients were followed up for a median time of 5 months (range, 2-14 months). Five patients died with 30-day mortality of 9.1%(5/55) with in postoperative 30 days. Abdominal pain did not recur in other patients. During postoperative month 5, 3 patients suffered from abdominal pain and were confirmed not caused by superior mesenteric artery ischemia. Two patients with stent implantation had no recurrence during the follow-up 9 months. The rest patients showed no recurrence of superior mesenteric artery ischemia. Conclusion Endovascular interventional treatment can restore the intestinal blood supply quickly and reduce mortality, and is safe and feasible treatment method for superior mesenteric artery ischemia. Key words: Superior mesenteric artery ischemia; Endovascular interventional therapy; Efficacy

English

INTRODUCTION: Gall Bladder perforation with superior mesenteric artery thrombosis causing midgut gangrene are two different pathologies occurring in a patient at same time presenting as an acute abdomen is a rare case. There is no such case reported in the literature of these two different diseases occurring together at a time in a patient. Incidence of isolated Gall Bladder perforation is reported as 3 % in cases of acute cholecystitis with mortality ranging from 12 to 16%1. Superior mesenteric artery ischemia is due to sudden hypoperfusion of small intestine leading eventually to small bowel gangrene. Acute mesenteric ischemia is a lethal disease due to delay in diagnosis by virtue of its nonspecific clinical presentation. Incidence of both the pathologies in a single patient has not been documented till date, however awareness of condition with high index of suspicion and early intervention is needed as emphasized in our case.

Percutaneous mechanical thrombectomy of superior mesenteric artery embolism

BackgroundThe present series present three consecutive cases of successful percutaneous mechanical embolectomy in acute superior mesenteric artery ischemia. Superior mesenteric artery embolism is a rare abdominal emergency that commonly leads to bowel infarction and has a very high mortality rate. Prompt recognition and treatment are crucial for successful outcome. Endovascular therapeutic approach in patients with acute SMA embolism in median portion of its stem is proposed.Case reports.Three male patients had experienced a sudden abdominal pain and acute superior mesenteric artery embolism in median portion of its stem was revealed on computed tomography angiography. No signs of intestinal infarction were present. The decision for endovascular treatment was made in concordance with the surgeons. In one patient 6 French gauge Rotarex® device was used while in others 6 French gauge Aspirex® device were used. All patients experienced sudden relief of pain after the procedure with no signs of intestinal infarction. Minor procedural complication – rupture of a smaller branch of SMA during Aspirex® treatment was successfully managed by coiling while transient paralytic ileus presented in one patient resolved spontaneously. All three patients remained symptom-free with patent superior mesenteric artery during the follow-up period.ConclusionsPercutaneous mechanical thrombectomy seems to be a rapid and effective treatment of acute superior mesenteric artery embolism in median portion of its stem in absence of bowel necrosis. Follow-up of our patients showed excellent short- and long-term results.

Successful recanalization of acute superior mesenteric artery ischemia with balloon angioplasty and aspiration embolectomy

Successful recanalization of acute superior mesenteric artery ischemia with balloon angioplasty and aspiration embolectomy

Critical role of interleukin-17A in murine intestinal ischemia-reperfusion injury

Intestinal ischemia-reperfusion (I/R) injury causes severe illness frequently complicated by remote multiorgan dysfunction and sepsis. Recent studies implicated interleukin-17A (IL-17A) in regulating inflammation, autoimmunity, and I/R injury. Here, we determined whether IL-17A is critical for generation of intestinal I/R injury and subsequent liver and kidney injury. Mice subjected to 30 min of superior mesenteric artery ischemia not only developed severe small intestinal injury (necrosis, apoptosis, and neutrophil infiltration) but also developed significant renal and hepatic injury. We detected large increases in IL-17A in the small intestine, liver, and plasma. IL-17A is critical for generating these injuries, since genetic deletion of IL-17A- or IL-17A-neutralizing antibody treatment markedly protected against intestinal I/R injury and subsequent liver and kidney dysfunction. Intestinal I/R caused greater increases in portal plasma and small intestine IL-17A, suggesting an intestinal source for IL-17A generation. We also observed that intestinal I/R caused rapid small intestinal Paneth cell degranulation and induced murine α-defensin cryptdin-1 expression. Furthermore, genetic or pharmacological depletion of Paneth cells significantly attenuated the intestinal I/R injury as well as hepatic and renal dysfunction. Finally, Paneth cell depletion significantly decreased small intestinal, hepatic, and plasma IL-17A levels after intestinal I/R. Taken together, we propose that Paneth cell-derived IL-17A may play a critical role in intestinal I/R injury as well as extraintestinal organ dysfunction.

Isoflurane Post-conditioning Protects Against Intestinal Ischemia-Reperfusion Injury and Multiorgan Dysfunction via Transforming Growth Factor-β1 Generation

This study examined volatile anesthetic-mediated protection against intestinal ischemia-reperfusion injury (IRI). Intestinal IRI is a devastating complication in the perioperative period leading to systemic inflammation and multiorgan dysfunction. Volatile anesthetics, including isoflurane, have anti-inflammatory effects. We aimed to determine whether isoflurane, given after intestinal ischemia, protects against intestinal IRI and the mechanisms involved in this protection. : After IACUC approval, mice were anesthetized with pentobarbital and subjected to 30 minutes of superior mesenteric artery ischemia, followed by 4 hours of equianesthetic doses of pentobarbital or isoflurane. Five hours after reperfusion, small intestine tissues were analyzed for morphological injury, apoptosis, neutrophil infiltration, proinflammatory mRNAs, and TGF-(Transforming Growth Factor-)β1 levels. We also assessed hepatic and renal injury after intestinal IRI. Intestinal IRI with pentobarbital led to significant small intestinal dysfunction with increased mucosal injury, TUNEL (transferase biotin-dUTP nick end-labeling)-positive cells, neutrophil infiltration, and proinflammatory mRNAs as well as elevated plasma alanine aminotransferase and creatinine levels. Isoflurane exposure after IRI led to significant attenuation of intestinal, hepatic, and renal injuries. Furthermore, the protective effects of isoflurane were abolished by treatment with a TGF-β1 neutralizing antibody before induction of IRI. Finally, isoflurane exposure led to increased TGF-β1 levels in intestinal epithelial cells and in plasma. Our findings demonstrate that isoflurane post-conditioning protects against small intestinal injury and hepatic and renal dysfunction after severe intestinal IRI via induction of intestinal epithelial TGF-β1. Our findings support therapeutic applications of volatile anesthetics during the intraoperative and postoperative periods and imply an important role of TGF-β1 signaling in modulating multiorgan injury.

Analysis of serum enzyme levels in a rabbit model of acute mesenteric ischemia

Early diagnosis of acute mesenteric ischemia (AMI) remains very difficult, partly due to the fact that useful markers of early small bowel ischemia have not yet been identified. Thus, in this study, we aimed to evaluate the levels of serum intracellular enzymes in the tissues and organs in a controlled animal model of mesenteric intestinal ischemia. Forty-eight New Zealand rabbits were divided into 4 groups including the control, artery ligation, vein ligation, and both artery and vein ligation groups. Plasma samples were obtained at 0-, 1-, 3-, 6- and 9-h time-points and enzyme levels were determined. The bowel color and vitality were observed at the same time. The bowel showed an appearance of infarction after a period of ischemia in the animals. Six and 9 h after superior mesenteric artery ischemia, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels increased significantly. However, after 3 h of superior mesenteric venous (SMV) ligation, γ-glutamyl transpeptidase levels in the blood were considerably higher compared to the control group. Six hours after SMV ischemia, ALT, AST, alkaline phosphatase and lactate dehydrogenase levels were significantly elevated compared to those pre-ligation. Serum enzyme levels during intestinal ischemia are not able to provide sufficient information as regards the extent and reversibility of intestinal ischemia, although, they may be able to reflect the presence of injury.

A Novel ELR-CXC Chemokine Antagonist Reduces Intestinal Ischemia Reperfusion-Induced Mortality, and Local and Remote Organ Injury

Neutrophil sequestration plays an important role in mediating local and remote organ injury induced by ischemia and reperfusion (I/R). The Glu-Leu-Arg (ELR)-CXC subfamily of chemokines, all CXCR1 or CXCR2 ligands, are primary agonists for such neutrophil recruitment. Herein, we assessed the effects of a combined CXCR1/CXCR2 antagonist, CXCL8((3-72))K11R/G31P (G31P), on neutrophilic local (gut) and distant organ injury and outcomes after superior mesenteric artery I/R in rats. Male Sprague-Dawley rats (n=6-10) were subjected to either sham treatment or superior mesenteric artery ischemia for 1h; all animals received either saline or G31P (500 mug/kg, s.c.) and were euthanized for assessment after either 2 or 5h of arterial reperfusion. Survival and gut pathology, and pulmonary neutrophils were assessed directly, while bronchoalveolar lavage (BAL) fluid total protein levels and red blood cell (RBC) numbers were determined by protein assay and direct counting. Expression of inflammatory mediators in the lung and jejunum was measured by quantitative RT-PCR, colorimetric or gel zymography assays. Sham treatment animals suffered no discernible gut or pulmonary pathology. At 2 and 5h after reperfusion, the survival levels of the saline-treated I/R injury animals were 80% and 50%, respectively, while all G31P-treated animals survived. I/R injury led to substantial villous pathology within the jejunum, and G31P significantly reduced these pathology scores as well as neutrophil infiltration of the jejunal lamina propria and lung parenchyma, and vascular leakage into the airways (BAL protein). The tissue injury increased expression of myeloperoxidase and matrix metalloproteinase (MMP)-2 and MMP-9 in the gut tissues, but G31P treatment did not significantly affect this response. Intestinal I/R increased expression of IL-1, IL-6, GRO, and MIP-2 in the ischemic jejunum and the lung tissues, but here too G31P treatment had no palliative effects on these responses. These results suggest that full-spectrum ELR-CXC chemokine antagonism has significant protective effects against I/R-induced local and remote organ injury.

Experience in the management of acute superior mesenteric artery ischemia

To study the management of acute superior mesenteric artery (SMA) ischemia and to improve its prognosis. The clinical data of 37 patients treated from January 1996 to August 2007 was retrospectively reviewed. Of the cases, 19 (51.4%) patients were diagnosed with acute SMA embolism, 15 (40.5%) with acute SMA thrombosis, 2 (5.4%) with spontaneous isolated dissection of SMA and 1 (2.7%) with SMA aneurysm. Nineteen (51.4%) patients were misdiagnosed in emergency. Eighteen (48.6%) patients died in the hospital, and most of them died of severe infection and multiple organ failure. Three cases of the survived 19 patients experienced severe complications (2 with short gut syndrome, 1 with cerebral hemorrhage). Nine cases were followed-up for a mean period of 15 months, and 5 died during that term. Acute SMA ischemia has multiple etiological factors. Early intervention can improve the prognosis.

Mesenteric Artery Occlusion Secondary to Activated Protein C Resistance

We present a case of mesenteric ischemia in a 32-year-old woman. The rarity of this potentially fatal condition in this age group, the diagnostic and therapeutic challenges associated with such a condition, and secondary causes that must always be investigated are highlighted. In this case, activated protein C resistance resulted in thrombosis of the superior mesenteric artery and subsequent bowel ischemia.

Changes in intestinal motility and in the myenteric plexus in a rat model of intestinal ischemia–reperfusion

Background/Purpose Early histologic changes induced by intestinal ischemia–reperfusion injury (IIRI) have been extensively studied using animal models. However, information regarding late effects on intestinal motility is lacking. The aim of this study was to investigate the late effects of IIRI on myenteric plexus histology and intestinal motility. Materials and Methods Thirty-two postweaning male mice weighing between 58 and 103 g were divided randomly into 4 groups: Control (unoperated), Sham (celiotomy), 30-minute ischemia (celiotomy and superior mesenteric artery ischemia for 30 minutes), and 45-minute ischemia (celiotomy and superior mesenteric artery ischemia for 45 minutes). Postoperative intestinal motility was assessed by weighing total fecal output for 24 hours on the 3rd, 7th, 14th, and 21st day after surgery. Segments of duodenum, jejunum, and ileum were examined at light microscopy for changes in the myenteric plexus. Results Three weeks after IIRI, the ganglion cells from the myenteric plexus appeared in light microscopy, spongy or foamy, containing many vacuoles in their cytoplasm. The neuronal nucleus became irregular, with degenerative signs. These alterations did not occur among animals from the control or sham groups. Although the animals of the 45-minute ischemia group showed a significant drop in fecal output in the 21st postoperative day, this appeared to have no effect on weight gain. Conclusions The results suggest that intestinal ischemia–reperfusion causes late neuronal damage. These changes resulted in alterations of intestinal motility, which, within the conditions of the present study, had no repercussion on general weight gain.

Occurrence and functional consequences of shunting of the microcirculation after mesenteric ischemia

Shunting of the microcirculation contributes to the pathology of sepsis and septic shock. In this study, we hypothesize that shunting of the microcirculation occurs after superior mesenteric artery (SMA) ischemia (occlusion) and reperfusion, and we explore functional consequences using intravital microscopy. Spontaneously breathing animals (rats) (n = 30) underwent occlusion of the SMA for 0 (controls), 30 or 60 minutes followed by reperfusion (4 hours) with normal saline. Leukocyte–endothelial interactions in mesenteric venules were quantified in an exteriorized ileal loop using intravital microscopy. Abdominal blood flow was recorded continuously, and arterial blood gases were analyzed at intervals. Continuous SMA blood flow measurements were performed in comparable groups without exteriorizing an ileal loop. Adherent leukocytes increased shortly after reperfusion in ischemia groups, and plateaued in these groups. The centerline velocity and shear rate in the recorded venules were significantly reduced after reperfusion down to low-flow/no-flow in animals undergoing 60 minutes of mesenteric artery occlusion compared with animals with 30 minutes occlusion and controls, whereas perfusion of the SMA and ileal vessels persisted. The microcirculatory changes in animals with 60 minutes occlusion were accompanied by progressive metabolic acidosis, substantially larger volumes of intravenous fluids needed to support arterial blood pressure and significantly reduced survival (30%). In the groups with continuous SMA blood flow measurements, SMA blood flow increased in relation to abdominal blood flow after reperfusion in animals with 60 minutes occlusion, and remained constant in animals undergoing 30 minutes occlusion and controls. Survival was 80% in animals with 60 minutes occlusion without an exteriorized ileal loop. SMA occlusion for 60 minutes and subsequent reperfusion causes perfusion abnormalities in the mesenteric microcirculation as often seen in sepsis and septic shock with increased microcirculation shunting, progressive metabolic acidosis and increased mortality. To detect these significant changes requires prolonged observation periods and might help to find new treatments to improve the poor prognosis of mesenteric ischemia.

L-arginine protects the mesenteric vascular circulation against cardiopulmonary bypass-induced vascular dysfunction

Background. The aim of our study was to determine whether addition of the nitric oxide donor l-arginine at reperfusion may prevent the cardiopulmonary bypass (CPB)-induced vascular alterations in the intestine. Methods. Twelve dogs underwent 90-minute hypothermic CPB. After 60 minutes, the cardiac arrest-treated group (n = 6) received 40 mg/kg intravenous bolus l-arginine, followed by 3 mg/kg/min infusion for 20 minutes. Hemodynamic parameters, blood gases, lactate, and glucose were monitored. Reactive hyperemia (RH) in response to superior mesenteric artery ischemia and vasorelaxation to systemically administered vasoactive drugs (acetylcholine [ACH] and sodium nitroprusside) were assessed before and after CPB and defined as percent change of vascular resistance. Results. In the control group, CPB reduced reactive hyperemia (RH) (−26 ± 15% vs −53 ± 5%), and the response to ACH (−30 ± 3% vs −42 ± 7%). In the treated group, the post-CPB endothelial dysfunction was reversed (−37 ± 1%, P <.05 vs control group) and RH partially recovered (−34 ± 4%, P <.05). Administration of l-arginine resulted in a higher mesenteric oxygen delivery, increased nitrite/nitrate production, and lower lactate release from the mesenteric vascular circulation after reperfusion. Conclusions. CPB disrupts some of the regulatory functions of the endothelial cell in the mesenterium and these are mostly related to nitric oxide unavailability. Systemic supplementation of l-arginine at reperfusion prevents the CPB-induced mesenteric endothelial dysfunction in association with an increased blood distribution and a reduced metabolic impairment. (Surgery 2003; 134:72-9.)

Short-term intestinal ischemia-reperfusion alters intestinal motility that can be preserved by xanthine oxidase inhibition.

While the effects of transient intestinal ischemia on mucosa have been well investigated, less is known about its effect on motor function. An experimental study was designed to investigate the effects of ischemia-reperfusion (I/R) on intestinal motility and intestinal muscular microcirculation. Wistar albino rats were divided into four groups: (1) baseline, (2) sham operation, (3) I/R, and (4) I/R with allopurinol pretreatment. Ischemia was induced by clamping the superior mesenteric artery (SMA) for 10 min. Gastroanal transit time (GATT) was measured with serial x-rays after instillation of barium sulfate to the stomach. Intestinal muscular microcirculation was evaluated by determining the number of carbon-perfused intestinal muscular microvessels (CPIMM). I/R prolonged GATT and decreased CPIMM significantly (P < 0.01). Pretreatment with allopurinol prevented prolongation of GATT and returned the number of CPIMM to the level of sham treatment (P < 0.01). In conclusion, reperfusion after 10 min of SMA ischemia alters intestinal motility. The no-reflow phenomenon plays an important role in this alteration of motility. Administration of allopurinol before reperfusion preserves intestinal motility by preventing the occurrence of no-reflow phenomenon.