Natural History of Asymptomatic Superior Mesenteric Arterial Stenosis Depends on Coeliac and Inferior Mesenteric Artery Status.

OBJECTIVE: The benefit of preventive treatment for superior mesenteric artery (SMA) stenosis remains uncertain. The latest European Society for Vascular Surgery (ESVS) guidelines remain unclear given the lack of data in the literature. The aim of this study was to evaluate asymptomatic SMA stenosis prognosis according to the presence of associated coeliac artery (CA) and/or inferior mesenteric artery (IMA) stenosis. METHODS: This was a single academic centre retrospective study. The entire computed tomography (CT) database of a single tertiary hospital was reviewed from 2009 to 2016. Two groups were defined: patients with isolated > 70% SMA stenosis (group A) and patients with both SMA and CA and/or IMA > 70% stenosis (group B). Patient medical histories were reviewed to determine the occurrence of mesenteric disease (MD) defined as development of acute mesenteric ischaemia (AMI) or chronic mesenteric ischaemia (CMI). RESULTS: Seventy-seven patients were included. Median follow up was 39 months. There were 24 patients in group A and 53 patients in group B. In group B, eight (10.4%) patients developed MD with a median onset of 50 months. AMI occurred in five patients with a median of 33 months and CMI in three patients with a median of 88 months. Patients of group B developed more MD (0% vs. 15.1%; p = .052). The five year survival rate was 45% without significant difference between groups. CONCLUSION: Patients with SMA stenosis associated with CA and/or IMA seem to have a higher risk of developing mesenteric ischaemia than patients with isolated SMA stenosis. Considering the low life expectancy of these patients, cardiovascular risk factor assessment and optimisation of medical treatment is essential. Preventive endovascular revascularisation could be discussed for patients with non-isolated > 70% SMA stenosis, taking into account life expectancy.

Vascular Calcifications are Associated with Increased Mortality in Patients with Acute Mesenteric Ischemia.

BACKGROUND: Vascular calcifications have been identified as predictors of mortality in several cardiovascular diseases but have not been investigated in context of acute mesenteric ischemia. The aim of this study was to investigate the impact of vascular calcifications in patients with acute mesenteric ischemia. METHODS: Patients admitted for an acute mesenteric ischemia were retrospectively included. The presence of calcifications in the visceral aorta, the celiac trunk, the superior mesenteric artery, and the renal arteries was assessed on computed tomography scan images at the arterial phase. The calcification volumes were measured using the software Aquarius iNtuition Edition®. RESULTS: The all-cause mortality was 55 out of 86 patients (63.9%) for a median follow-up of 3.5 days (1-243). The survival rate of patients with calcification in the superior mesenteric artery was significantly lower than that of those without calcification (22% vs. 55.6%, P = 0.019). Patients who died had significantly a higher frequency of calcifications in the superior mesenteric artery, the visceral aorta, the celiac trunk, and the renal arteries. CONCLUSIONS: The presence of vascular calcifications in the superior mesenteric artery is associated with increased mortality in patients diagnosed with acute mesenteric ischemia. Further studies are required to identify the mechanisms underlying this association.

Mesoportal bypass, interposition graft, and mesocaval shunt: Surgical strategies to overcome superior mesenteric vein involvement in pancreatic cancer.

BACKGROUND: In pancreatic cancer, extensive tumor involvement of the mesenteric venous system poses formidable challenges to operative resection. Such involvement can result from cavernous collateral veins leading to increased intraoperative blood loss or long-segment vascular defects of not only just the superior mesenteric vein but also even jejunal/ileal branches. Strategies to facilitate margin-free resection and safe vascular reconstruction in pancreatic surgery are important, particularly because systemic control of the tumor is improving with multi-agent chemotherapy regimens. METHODS: We describe a systematic, multidisciplinary assessment for patients with pancreatic cancer that involves the superior mesenteric vein, as well as the preoperative planning of those undergoing operative resection. In addition, detailed descriptions of operative approaches and technical strategies, which evolved with increasing experience at a high-volume center, are presented. RESULTS: For the preoperative evaluation of tumor-free, vascular locations for potential reconstruction and collateralization, computed tomographic imaging with high-resolution of vascular structures (used with 3-dimensional or cinematic rendering) allows a precise calibration of radiographic data with intraoperative findings. From an operative perspective, we identified 5 potential strategies to consider for resection: collateral preservation, mesoportal bypass (preresection), mesoportal interposition graft (postresection), mesocaval shunt, and various combinations of these strategies. Many of these techniques use interposition grafts, making it essential to assess autologous veins (preferred conduit for reconstruction) or to prepare cryopreserved vascular allografts (an alternative conduit, which must be thawed and should be matched for size and blood type). CONCLUSION: Herein we share operative strategies to overcome involvement of the superior mesenteric vein in pancreatic cancer. Improvements in preoperative planning and operative technique can address common barriers to resection with curative intent.

Quantitative evaluation of superior mesenteric artery calcification in hemodialysis patients undergoing aortic valve replacement.

OBJECTIVE: Postoperative acute mesenteric ischemia (AMI) in the long-term hemodialysis (HD) patients could be a disastrous complication leading to high mortality. The objective is to evaluate the association between the presence of superior mesenteric artery calcification (SMAC) and early and late outcomes after aortic valve replacement (AVR) in HD patients. METHODS: Between April 2003 and December 2018, the enrolled 46 HD patients (19 women; mean age 72 years) who underwent AVR for severe aortic valve stenosis were retrospectively reviewed. 25 patients (54.3%) who had severe calcifications of superior mesenteric artery (SMA) were defined as the SMAC group, and the calcification extent of SMA was evaluated on preoperative non-contrast CT using Agaston calcium score [calcification area (cm2) × max CT value (HU)]. The operative outcomes were compared with those of the non-SMAC group comprising 21 patients (45.7%). RESULTS: The following factors in SMAC group were statistically higher compared with those of the non-SMAC group: age (73.6 ± 7.2 vs 69.3 ± 7.1 years; p = 0.04), celiac artery calcification (76.4% vs 17.6%; p < 0.001), calcium score of SMA (692.3 ± 300.0 vs 123.5 ± 180.7; p < 0.001), the incidence of AMI (24.0% vs 4.7%; p = 0.001), and hospital mortality (16.0% vs 0%; p = 0.02). In multivariate analysis, the presence of SMAC was significantly associated with AMI (OR 3.8, p = 0.05) and hospital mortality (OR 2.4, p = 0.02). Calcium score of SMA in patients complicated with AMI was significantly higher than those without AMI (815.7 ± 300.5 vs 366.9 ± 351.2; p < 0.01). CONCLUSION: Quantitative evaluation of SMAC could be a predictive marker of incidence of AMI after AVR in HD patients.

Use of long saphenous vein graft in acute on chronic mesenteric ischaemia.

Acute mesenteric ischaemia is a relatively rare surgical emergency, but despite advances in diagnostic tests, the mortality of this condition remains stubbornly high (50%-80%). This is principally because of the non-specific nature of the presenting symptoms and subsequent delay in diagnosis. We report an unusual case of acute mesenteric ischaemia treated by emergency laparotomy, small bowel resection and revascularisation using reversed long saphenous vein graft.

Neutrophil-to-Lymphocyte Ratio and Platelet-to-Lymphocyte Ratio Are Effective Predictors of Prognosis in Patients with Acute Mesenteric Arterial Embolism and Thrombosis.

BACKGROUND: The neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) have been shown to be valuable prognostic markers for a variety of pathological conditions including solid tumors, sepsis, and others. However, the prognostic values of the NLR and PLR in patients with acute mesenteric arterial embolism (AMAE) and acute mesenteric arterial thrombosis (AMAT) have not been elucidated. The aim of this study was to determine the predictive value of the NLR and PLR for poor prognosis in patients with AMAE and AMAT. METHODS: A total of 137 patients with AMAE (n = 77) or AMAT (n = 60) were divided into a poor outcome group (cases of intestinal necrosis or death) and a better outcome group (cases without intestinal necrosis who survived successfully), according to prognosis. Neutrophil, platelet, and lymphocyte counts were recorded before pharmacotherapy or surgery. The NLR and PLR were calculated, and logistic regression analysis was performed to test their prognostic values. RESULTS: The cutoff values for NLR and PLR were 11.05 and 156.26, respectively. The PLR was linearly associated with the NLR (R = 0.769, P < 0.001). NLR (odds ratio [OR] = 6.835, 95% confidence interval [CI] = 2.282-20.469, P = 0.001), PLR (OR = 4.871, 95% CI = 1.627-14.587, P = 0.005), and coronary heart disease (OR = 3.388, 95% CI = 1.156-9.929, P = 0.026) were found to be independent prognostic factors for the patients. CONCLUSIONS: NLR ≥ 11.05, PLR ≥ 156.26, and coronary heart disease were shown to be risk factors for poor prognosis in patients with AMAE and AMAT. According to these factors, patients can be divided into 3 prognostic groups: good, NLR < 11.05 with PLR < 156.26; moderate, NLR < 11.05 with PLR ≥ 156.26 or NLR ≥ 11.05 with PLR < 156.26; and poor, NLR ≥ 11.05 with PLR ≥ 156.26.

Fatal Acute Hemorrhagic Bowel Infarction Caused by Mesenteric Venous Thrombosis.

Acute mesenteric venous thrombosis (MVT) is a rare, but life-threatening medical phenomenon. MVT is normally characterized by insidious onset, with nonspecific signs and symptoms. A high index of clinical suspicion is required for diagnosis, and emergency surgery is necessary to optimize the chances of patient survival, especially in the people aged more than 70 years. Surprisingly, based on my review of the literature, no fatal acute MVT case has been reported in the forensic literature. All reported such cases have been documented in medical literature, and most of them have been associated with underlying risk factors for venous thrombosis, such as hypercoagulable state, certain cancers, and stasis of the blood flow. Here, I report the case of a sudden unexpected death due to extensive intestinal ischemia and infarction with massive abdominal hemorrhage caused by acute MVT in a 72-year-old man without known underlying risk factors.

Idiopathic Myointimal Hyperplasia of Mesenteric Veins: An Uncommon Cause of Ischemic Colitis With Distinct Mucosal Features.

Idiopathic myointimal hyperplasia of mesenteric veins causes chronic ischemic mucosal injury with segmental strictures that mimic inflammatory bowel disease and nonocclusive ischemic colitis. It is characterized by myointimal proliferative changes that narrow the lumina of veins combined with ischemic injury and ulcers. Most cases reported to date have been diagnosed following surgical resection. The aim of this study was to determine whether mucosal changes of idiopathic myointimal hyperplasia of mesenteric veins are sufficiently sensitive and specific to allow its recognition in biopsy material. The study group consisted of 10 patients with idiopathic myointimal hyperplasia of mesenteric veins who underwent surgical resection of the affected colon, 7 of whom had available prior endoscopic biopsies. The control group included 10 patients each with radiation, nonocclusive ischemia, Crohn disease, diverticulitis, and mucosal amyloidosis, and 5 cases of small vessel (leukocytoclastic) vasculitis. Study patients were mostly older men with distal colorectal disease. All resection specimens showed mucosal ischemia with numerous thick-walled (arteriolized) capillaries and glassy subendothelial fibrin deposits; numerous hyalinized, eosinophilic thrombi were detected in 90% of colectomy specimens. Biopsies showed arteriolized capillaries (100%), subendothelial fibrin deposits (86%), fibrin thrombi (43%), and perivascular hyalinization (43%). Fibrin thrombi were observed in only one case each of ischemic colitis and small vessel vasculitis, and none of the other abovementioned features were seen in any of the controls. We conclude that arteriolized capillaries, subendothelial fibrin deposits, and perivascular hyalinization are frequent and specific features that can facilitate recognition of idiopathic myointimal hyperplasia of mesenteric veins in biopsy samples.

Mesenteric Arteriovenous Dysplasia/Vasculopathy Is Distinct From Fibromuscular Dysplasia.

Fibromuscular dysplasia (FMD) is a noninflammatory, nonatherosclerotic vasculopathy that usually affects the carotid and renal arteries. We have observed FMD-like vascular changes in specimens resected for ischemia or Crohn's disease (CD). On the basis of a systematic clinicopathologic review of these 11 cases identified between 1982 and 2014, we describe a distinct mesenteric vasculopathy that involves both arteries and veins [mesenteric arteriovenous dysplasia/vasculopathy (MAVD/V)] and is characterized by (1) concentric/eccentric smooth muscle collarette around the tunica media of both the artery and the vein in ≥2 foci, (2) varying degrees of intimal and medial hyperplasia and adventitial fibrosis, and (3) lack of inflammation or thrombi. MAVD/V cases were clinically diagnosed as CD (45%), mass/lesion (27%), ischemia (9%), obstruction (9%), or rectal prolapse (9%). Abdominal pain for >1 year was the most common symptom. Most patients were women (M:F=1:2.7; mean age, 63 y). Mucosal changes mimicking CD, such as architectural distortion (55%), multifocal ulcers (73%), and pyloric gland metaplasia (64%), were common; however, no granulomas or transmural lymphoid aggregates were identified. Ischemic pattern of injury was seen in 4 cases. Upon follow-up (mean, 31.2 mo), 8 patients were found to be asymptomatic, 2 had died of unrelated causes, and 1 was lost to follow-up. We propose the name MAVD/V for a distinct noninflammatory, nonatherosclerotic, localized form of mesenteric vasculopathy that involves both arteries and veins, distinct from FMD. Unlike FMD, surgical resection appears to be curative, with a favorable clinical outcome. Awareness of this vascular entity is important as patients may be potentially misdiagnosed as having CD and ischemic bowel disease.

Endothelial Cell-Derived von Willebrand Factor Is the Major Determinant That Mediates von Willebrand Factor-Dependent Acute Ischemic Stroke by Promoting Postischemic Thrombo-Inflammation.

OBJECTIVE: von Willebrand factor (VWF), which is synthesized in endothelial cells and megakaryocytes, is known to worsen stroke outcome. In vitro studies suggest that platelet-derived VWF (Plt-VWF) is biochemically different from the endothelial cell-derived VWF (EC-VWF). However, little is known about relative contribution of different pools of VWF in stroke. APPROACH AND RESULTS: Using bone marrow transplantation, we generated chimeric Plt-VWF mice, Plt-VWF mice that lack ADAMTS13 in platelets and plasma (Plt-VWF/Adamts13(-/-)), and EC-VWF mice to determine relative contribution of different pools of VWF in stroke. In brain ischemia/reperfusion injury model, we found that infarct size and postischemic intracerebral thrombo-inflammation (fibrin(ogen) deposition, neutrophil infiltration, interleukin-1ß, and tumor necrosis factor-α levels) within lesions were comparable between EC-VWF and wild-type mice. Infarct size and postischemic thrombo-inflammation were comparable between Plt-VWF and Plt-VWF/Adamts13(-/-) mice, but decreased compared with EC-VWF and wild-type mice (P<0.05) and increased compared with Vwf(-/-) mice (P<0.05). Susceptibility to FeCl3 injury-induced carotid artery thrombosis was comparable between wild-type and EC-VWF mice, whereas Plt-VWF and Plt-VWF/Adamts13(-/-) mice exhibited defective thrombosis. Although most of the injured vessels did not occlude, slope over time showed that thrombus growth rate was increased in both Plt-VWF and Plt-VWF/Adamts13(-/-) mice compared with Vwf(-/-) mice (P<0.05), but decreased compared with wild-type or EC-VWF mice. CONCLUSIONS: Plt-VWF, either in presence or absence of ADAMTS13, partially contributes to VWF-dependent injury and postischemic thrombo-inflammation after stroke. EC-VWF is the major determinant that mediates VWF-dependent ischemic stroke by promoting postischemic thrombo-inflammation.

A Case of Idiopathic Mesenteric Phlebosclerosis with Progressive Intestinal Necrosis.

The patient was a 39-year-old woman who was referred to our department from her previous doctor with a 2-day history of right abdominal pain. Abdominal computed tomography showed wall thickening associated with calcification in the ascending colon. Contrast enhancement in the same portion of the intestinal wall was rather poor. Fluid accumulation was also seen around the intestine, so emergency surgery was performed under a provisional diagnosis of intestinal necrosis. Intestinal necrosis due to idiopathic mesenteric phlebosclerosis was diagnosed from postoperative histopathological tests. Idiopathic mesenteric phlebosclerosis displays a chronic course and in most cases conservative treatment is indicated. Bowel obstruction is common among patients who require surgical treatment, but rare cases such as the present one are also seen in which intestinal necrosis occurs. In recent years, an association with herbal medicine has been indicated as one potential cause of this disease, and this entity should be kept in mind when patients with acute abdomen and a history of taking herbal medicines are encountered.

Embolic superior mesenteric artery (SMA) occlusion secondary to a cardiac sarcoma.

We present a case of embolic acute mesenteric ischaemia (AMI) secondary to an underlying cardiac sarcoma, an exceedingly rare presentation only reported twice before. A 46-year-old man presented to accident and emergency department during the night with severe abdominal pain and vomiting. An urgent CT angiograph demonstrated superior mesenteric artery (SMA) occlusion with ischaemic small bowel. Joint surgical effort from vascular and general surgeons successfully recanalised the SMA and a 20 cm segment of small bowel was resected. Postoperatively, an echocardiogram demonstrated a mass within the left atrium. After cardiothoracic resection, the mass was found to be a rare undifferentiated cardiac sarcoma. Further staining on the embolus retrieved from the SMA revealed scattered spindle cells with a similar immunohistochemistry profile to that of the resected cardiac sarcoma. The patient was subsequently discharged well on lifelong warfarin.

Intestinal Infarction Through Arterial Vascular Obstruction - Case Series from 1st and 3rd Surgery Clinics Cluj-Napoca.

This article presents a case series of intestinal infarction through obstruction of superior mesenteric artery - two cases of acute mesenteric artery embolism, two cases of acute mesenteric artery thrombosis and a case of volvulus.

Protective role of adiponectin in a rat model of intestinal ischemia reperfusion injury.

AIM: To determine the potential protective role of adiponectin in intestinal ischemia reperfusion (I/R) injury. METHODS: A rat model of intestinal I/R injury was established. The serum level of adiponectin in rats with intestinal I/R injury was determined by enzyme-linked immunosorbent assay (ELISA). The serum levels of interleukin (IL)-1ß, IL-6, and tumor necrosis factor (TNF)-α were also measured by ELISA. Apoptosis of intestinal cells was detected using the terminal deoxynucleotidyl transferase dUTP nick end labeling assay. The production of malondialdehyde (MDA) and superoxide dismutase (SOD) and villous injury scores were also measured. RESULTS: Adiponectin was downregulated in the serum of rats with intestinal I/R injury compared with sham rats. No significant changes in the expression of adiponectin receptor 1 and adiponectin receptor 2 were found between sham and I/R rats. Pre-treatment with recombinant adiponectin attenuated intestinal I/R injury. The production of pro-inflammatory cytokines, including IL-6, IL-1ß, and TNF-α, in rats with intestinal I/R injury was reduced by adiponectin pre-treatment. The production of MDA was inhibited, and the release of SOD was restored by adiponectin pre-treatment in rats with intestinal I/R injury. Adiponectin pre-treatment also inhibited cell apoptosis in these rats. Treatment with the AMP-activated protein kinase (AMPK) signaling pathway inhibitor, compound C, or the heme oxygenase 1 (HO-1) inhibitor, Snpp, attenuated the protective effects of adiponectin against intestinal I/R injury. CONCLUSION: Adiponectin exhibits protective effects against intestinal I/R injury, which may involve the AMPK/HO-1 pathway.

TLR4-HMGB1-, MyD88- and TRIF-dependent signaling in mouse intestinal ischemia/reperfusion injury.

AIM: To characterize high-mobility group protein 1-toll-like receptor 4 (HMGB1-TLR4) and downstream signaling pathways in intestinal ischemia/reperfusion (I/R) injury. METHODS: Forty specific-pathogen-free male C57BL/6 mice were randomly divided into five groups (n = 8 per group): sham, control, anti-HMGB1, anti-myeloid differentiation gene 88 (MyD88), and anti-translocating-chain-associating membrane protein (TRIF) antibody groups. Vehicle with the control IgG antibody, anti-HMGB1, anti-MyD88, or anti-TRIF antibodies (all 1 mg/kg, 0.025%) were injected via the caudal vein 30 min prior to ischemia. After anesthetization, the abdominal wall was opened and the superior mesenteric artery was exposed, followed by 60 min mesenteric ischemia and then 60 min reperfusion. For the sham group, the abdominal wall was opened for 120 min without I/R. Levels of serum nuclear factor (NF)-κB p65, interleukin (IL)-6, and tumor necrosis factor (TNF)-α were measured, along with myeloperoxidase activity in the lung and liver. In addition,morphologic changes that occurred in the lung and intestinal tissues were evaluated. Levels of mRNA transcripts encoding HMGB1 and NF-κB were measured by real-time quantitative PCR, and levels of HMGB1 and NF-κB protein were measured by Western blot. Results were analyzed using one-way analysis of variance. RESULTS: Blocking HMGB1, MyD88, and TRIF expression by injecting anti-HMGB1, anti-MyD88, or anti-TRIF antibodies prior to ischemia reduced the levels of inflammatory cytokines in serum; NF-κB p65: 104.64 ± 11.89, 228.53 ± 24.85, 145.00 ± 33.63, 191.12 ± 13.22, and 183.73 ± 10.81 (P < 0.05); IL-6: 50.02 ± 6.33, 104.91 ± 31.18, 62.28 ± 6.73, 85.90 ± 17.37, and 78.14 ± 7.38 (P < 0.05); TNF-α, 43.79 ± 4.18, 70.81 ± 6.97, 52.76 ± 5.71, 63.19 ± 5.47, and 59.70 ± 4.63 (P < 0.05) for the sham, control, anti-HMGB1, anti-MyD88, and anti-TRIF groups, respectively (all in pg/mL).Antibodies also alleviated tissue injury in the lung and small intestine compared with the control group in the mouse intestinal I/R model. The administration of anti-HMGB1, anti-MyD88, and anti-TRIF antibodies markedly reduced damage caused by I/R, for which anti-HMGB1 antibody had the most obvious effect. CONCLUSION: HMGB1 and its downstream signaling pathway play important roles in the mouse intestinal I/R injury, and the effect of the TRIF-dependent pathway is slightly greater.

Effect of protective solutions and hydroxyethyl starch in the attenuation of the injuries of ischemia and reperfusion of splanchnic organs

PURPOSE: Vogt´s antioxidant solution (red blood cells, Ringer's solution, sodium bicarbonate, mannitol, allopurinol and 50% glucose) or its modification including hydroxyethyl starch (HES) were tested for the prevention of splanchnic artery occlusion shock. METHODS: Seventy rats were distributed in treatment (3), control (1), and sham (3) groups. Ischemia and reperfusion were induced by celiac, superior mesenteric and inferior mesenteric arteries occlusion for 40 min, followed by 60 min reperfusion or sham procedures. Controls received saline, both treatment and sham groups received the Vogt's solution, modified Vogt's solution (replacing Ringer's solution by HES), or HES. Mean arterial blood pressure (MABP), ileal malondialdehyde (MDA) and plasmatic MDA were determined, and a histologic grading system was used. RESULTS: At reperfusion, MABP dropped in all I/R groups. Only HES treatment was able to restore final MABP to the levels of sham groups. Plasmatic MDA did not show differences between groups. Ileum MDA was significantly higher in the control and treatment groups as compared to the sham group. Histology ranking was higher in the only in control group. CONCLUSIONS: Hydroxyethyl starch was able to prevent hemodynamic shock but not intestinal lesions. Both treatments with Vogt's solutions did not show any improvement. .

Very short cycles of postconditioning have no protective effect against reperfusion injury. Experimental study in rats / Ciclos muito curtos de pós-condicionamento não protegem contra lesão de reperfusão. Estudo experimental em ratos

Introduction: Ischemic postconditioning has been recognized as effective in the prevention of reperfusion injury in situations of ischemia and reperfusion in various organs and tissues. However, it remains unclear what would be the best way to accomplish it, since studies show great variation in the method of their application. Objective: To assess the protective effect of ischemic postconditioning on ischemia and reperfusion in rats undergoing five alternating cycles of reperfusion and ischemia of 30 seconds each one. Methods: We studied 25 Wistar rats distributed in three groups: group A (10 rats), which underwent mesenteric ischemia (30 minutes) and reperfusion (60 minutes); Group B (10 rats), undergoing ischemia (30 minutes) and reperfusion (60 minutes), intercalated by postconditioning (5 alternating cycles of reperfusion and ischemia of 30 seconds each one); and group C - SHAM (5 rats), undergoing only laparotomy and manipulation of mesenteric artery. All animals underwent resection of an ileum segment for histological analysis. Results: The mean lesions degree according to Chiu et al. were: group A, 2.77, group B, 2.67 and group C, 0.12. There was no difference between groups A and B (P>0.05). Conclusion: Ischemic postconditioning was not able to minimize or prevent the intestinal tissue injury in rats undergoing ischemia and reperfusion process when used five cycles lasting 30 seconds each one. .

Introdução: O pós-condicionamento isquêmico tem sido reconhecido como eficaz na prevenção das lesões de reperfusão em situações de isquemia e reperfusão em vários órgãos e tecidos. Entretanto, não está ainda claro qual seria a melhor maneira de realizá-lo, já que as publicações mostram grande variação de método no seu emprego. Objetivo: Avaliar o efeito protetor do pós-condicionamento isquêmico na isquemia e reperfusão intestinal em ratos, através de cinco ciclos alternados de 30 segundos de isquemia e 30 segundos de reperfusão. Métodos: Foram estudados 25 ratos Wistar, distribuídos em três grupos: grupo A (10 ratos), em que se realizou isquemia (30 minutos) e reperfusão (60 minutos) mesentérica; grupo B (10 ratos), isquemia e reperfusão, seguidos de pós-condicionamento isquêmico com 5 ciclos alternados de reperfusão e reoclusão, de 30 segundos cada; e grupo C (5 ratos), controle (SHAM). Ao final, ressecou-se um segmento do intestino delgado para análise histológica. Avaliaram-se os resultados pela classificação de Chiu et al. e procedeu-se ao tratamento estatístico. Resultados: As médias dos graus de lesão tecidual segundo a classificação de Chiu et al. foram: no grupo A, 2,77; no grupo B, 2,67; e no grupo C, 0,12. A diferença entre o resultado do grupo A com o resultado do grupo B não teve significância estatística (P>0,05). Conclusão: O pós-condicionamento isquêmico não foi capaz de minimizar ou prevenir a lesão tecidual intestinal de ratos submetidos ao processo de isquemia e reperfusão mesentérica quando utilizados cinco ciclos com duração de 30 segundos cada. .

Protective effects of osthole on intestinal ischemia-reperfusion injury in mice.

OBJECTIVES: The purpose of this study was to evaluate the effect of intravenous injection of osthole on intestinal ischemia-reperfusion injury and parameters of oxidative stress. MATERIALS AND METHODS: In 45 Kunming male mice, treatment included sham surgery (15 mice); intestinal ischemia-reperfusion injury (clamping of the superior mesenteric artery, 2 h; clamp release, 1 h; 15 mice); or osthole treatment before and after ischemia-reperfusion injury (15 mice). Evaluation included histopathology, determination of intestinal wet/dry weight ratio, and measurement of levels of diamine oxidase, superoxide dismutase, malondialdehyde, interleukin 1ß, tumor necrosis factor α, and interleukin 2. Intestinal barrier permeability was evaluated with Evans blue test. RESULTS: The mean wet-to-dry weight ratio, Evans blue content, and Chiu score were significantly greater in the ischemia-reperfusion than in the sham group and lower in the osthole-treated than the ischemia-reperfusion group. The mean serum diamine oxidase, malondialdehyde, interleukin 1ß, and tumor necrosis factor α levels were significantly greater in the ischemia-reperfusion than in the sham group and lower in the osthole-treated than in the ischemia-reperfusion group. The mean superoxide dismutase activity and interleukin 2 levels were lower in the ischemia-reperfusion than in the sham group and greater in the osthole-treated than in the ischemia-reperfusion group. CONCLUSIONS: Treatment with osthole may protect against oxidative stress and tissue damage from intestinal ischemia-reperfusion injury.

Beneficial effects of intra-arterial and intravenous prostaglandin E1 in intestinal ischaemia-reperfusion injury.

OBJECTIVES: Ischaemia-reperfusion (I/R) injury is encountered in conditions that diminish intestinal blood flow. There is no clinically feasible technique available for mucosal preservation. METHODS: One hundred Wistar rats were subjected to intestinal ischaemia for 15 and 60 min (I15', I60'), followed by 1 and 7 days of reperfusion (R1d, R7d). Rats were subjected to ischaemia by clamping the superior mesenteric artery. Prostaglandin E1 (PGE1) (2.500 ng/kg intra-arterial bolus or 20 ng/kg intravenous infusion) was administered immediately prior to the commencement of the experimental period. Animals were divided into 20 groups: sham (laparotomy alone), sacrificed at 1 or 7 days; saline administration, 15 or 60 min of ischaemia, 1 or 7 days of reperfusion; prostaglandin E1 administration, 15 or 60 min of ischaemia, 1 or 7 days of reperfusion, each one for intra-arterial or intravenous administration. Ileal segments were excised and assessed for histopathological score, polymorphonuclear (PMN) leucocytes encountered and myeloperoxidase (MPO) activity measurement. RESULTS: I/R caused deterioration of histological characteristics. Prophylactic administration of PGE1 resulted in a significant decrease in the histological score compared with the respective saline group (analysis of variance, P < 0.005). In groups treated with PGE1, PMN leucocyte infiltration was lower for the 60 min of ischaemia group (I60'/R1d *P = 0.026; I60'/R7d P = 0.015). I15'/R7d did not lead to a significant reduction in PMN infiltration (P = 0.061). Pretreatment with PGE1 attenuates MPO levels after intestinal I/R injury (P < 0.05). No differences were encountered between types of administration. CONCLUSIONS: Results of this study showed that administration of prostaglandin E1 prevents I/R injury by diminishing histological damage parameters, inhibiting PMN leucocyte infiltration and attenuating MPO activity.

Mesenteric inflammatory veno-occlusive disease: radiographic and histopathologic evaluation of 2 cases.

Mesenteric inflammatory veno-occlusive disease (MIVOD) is a rare cause of inflammatory enterocolitis whose clinical and imaging presentation can be confused with mesenteric venous thrombosis and inflammatory bowel disease. We report two cases of histologically proven MIVOD in patients presenting with abdominal pain and describe potentially useful distinguishing features at contrast-enhanced CT, including prominent small pericolonic arteries and veins but a diminutive or absent inferior mesenteric vein. Alerting referring clinicians to the possibility of this diagnosis may help avoid unnecessary anticoagulation and reduce diagnostic delay. Treatment of MIVOD is surgical resection, which is typically curative.