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Portograma aéreo o portograma de aire (PA), se define como la presencia de aire en el sistema venoso portomesentérico. Neumatosis intestinal (NI) se define como la presencia de aire en la pared intestinal, independiente de su causa o localización. La principal etiología de estas alteraciones es la isquemia intestinal aguda y en general, se consideran predictores de perforación intestinal y de mal pronóstico. Un pequeño grupo de pacientes con PA y/o NI pueden evolucionar sin complicaciones e incluso cursan sin manifestaciones clínicas. Presentamos el caso de una paciente con antecedente quirúrgico inmediato de gastrectomía total y reconstrucción en Y de Roux, que evidenció en tomografía computarizada (TC) de abdomen de control PA y NI, sin alteraciones clínicas significativas asociadas. Hepatic portal venous gas (HPVG) is defined as the presence of air in the portal venous system. Pneumatosis intestinalis (PI) is defined as the presence of air within the bowel wall, regardless of its cause or location. Its main etiology is the intestinal ischemia and are generally considered predictors of intestinal perforation and wrong prognosis. A small group of patients with HPVG and PI may have a different clinical course, without complications and clinical manifestations. We report the case of a patient with immediate surgical history of total gastrectomy and Roux-en-Y reconstruction, which showed in computed tomography (CT) of the abdomen HPVG and PI, without associated clinically significant changes. © 2018, Sociedad Chilena de Radiologia. All rights reserved.

To investigate the role of interleukin (IL)-10 gene therapy on the reperfusion-induced lung injury, we utilised the technique of liposomal gene delivery before the induction of intestinal ischemia. Plasmid DNA encoding human IL10 (hIL-10) or empy vector was injected intraperitoneally 24 h before the study. Male Balb/c mice randomized into three groups: Sham operated control (n = 12), empty plasmid vector (n = 12), and hIL-10 gene therapy group (n = 12). The ischemia was generated by selective occlusion of superior mesenteric artery for 60 min. and followed by reperfusion for 30 min. Lung tissue neutrophil infiltration was determined by myeloperoxidase assay and neutrophil counts. For the determination of lung tissue microvascular permeability, Evans blue dye injection was made and the lung edema was assesed by wet/dry ratio. hIL-10 protein expression was studied by immunostaining and ELISA. We found that pre-ischemic hIL-10 overexpression attenuated dye extravasation, leukocyte sequestration and reduced pulmonary tissue injury compared to the empty vector-injected control. Our study indicates that pre-ischemic hIL-10 overexpression attenuates lung injury caused by intestinal ischemia-reperfusion. © 2005 Tohoku University Medical Press.

Trimetazidine (TMZ), a potent antioxidant agent, has been used to protect the myocardium, liver and kidney from ischemia reperfusion (IR) injury. We investigated the effect of TMZ, a cellular anti-ischemic agent and a free radical scavenger, on 60 min of warm intestinal IR injury in rats. Sprague-Dawley rats were divided into three groups: a sham-operated group (no IR injury, n = 8), an ischemic control group (control, n = 8), and a TMZ- treated group (3 mg/kg, n = 8). Malondialdehyde (MDA) levels, myeloperoxidase (MPO) activity, and mucosal damage were investigated after 120 min of reperfusion. MDA levels and MPO activity were more elevated and histopathological damage more severe in the control group than in the sham group (P < 0.05). MDA levels and MPO activity were lower and there was less histopathological damage in the TMZ group than in the control group (P < 0.05). Accumulation of lipid peroxidation products and neutrophils in mucosal tissues were significantly inhibited by TMZ treatment. We conclude that pretreatment of rats with TMZ before intestinal ischemia attenuates but does not prevent, histological damage.

Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-27T11:28:40Z No. of bitstreams: 0Bitstream added on 2014-05-27T14:42:55Z : No. of bitstreams: 1 2-s2.0-84874805360.pdf: 1394575 bytes, checksum: 573bfb2af4add411de8aa3a8efac6c77 (MD5) Made available in DSpace on 2014-05-27T11:28:40Z (GMT). No. of bitstreams: 0 Previous issue date: 2013-03-15 Background: Intestinal ischemia/reperfusion (IR) injury is a serious and triggering event in the development of remote organ dysfunction, from which the lung is the main target. This condition is characterized by intense neutrophil recruitment, increased microvascular permeability. Intestinal IR is also responsible for induction of adult respiratory distress syndrome, the most serious and life-threatening form of acute lung injury. The purpose of this study was to investigate the effect of annexin-A1 protein as an endogenous regulator of the organ remote injury induced by intestinal ischemia/reperfusion. Male C57bl/6 mice were subjected to intestinal ischemia, induced by 45 min occlusion of the superior mesenteric artery, followed by reperfusion. Results: The intestinal ischemia/reperfusion evoked a high intensity lung inflammation as indicated by the number of neutrophils as compared to control group. Treatment with annexin-A1 peptidomimetic Ac2-26, reduced the number of neutrophils in the lung tissue and increased its number in the blood vessels, which suggests a regulatory effect of the peptide Ac2-26 in the neutrophil migration. Moreover, the peptide Ac2-26 treatment was associated with higher levels of plasma IL-10. Conclusion: Our data suggest that the annexin-A1 peptidomimetic Ac2-26 treatment has a regulatory and protective effect in the intestinal ischemia/reperfusion by attenuation of the leukocyte migration to the lung and induction of the anti-inflammatory cytokine IL-10 release into the plasma. The anti-inflammatory action of annexin-A1 and its peptidomimetic described here may serve as a basis for future therapeutic approach in mitigating inflammatory processes due to intestinal ischemia/reperfusion. © 2013 Guido et al.; licensee BioMed Central Ltd. Department of Biology; Institute of Biosciences Letras e Ciências Exatas (IBILCE) São Paulo State University (UNESP), São José do Rio Preto, SP 15054-000 Department of Pharmacology Institute of Biomedical Sciences (ICB) University of São Paulo (USP), São Paulo, 05508-900 Department of Basic Science in Health Faculty of Medicine (FM) Federal University of Mato Grosso (UFMT), Mato Grosso, MT 78060-900 Department of Biology; Institute of Biosciences Letras e Ciências Exatas (IBILCE) São Paulo State University (UNESP), São José do Rio Preto, SP 15054-000

Background: Pyrrolidine dithiocarbamate (PDTC) is a low-molecular-weight thiol antioxidant and potent inhibitor of nuclear factor-κB (NF-κB) activation. It has been shown to attenuate harmful effects of ischemia/reperfusion (I/R) injury in many organs. In recent animal studies, destructive effects of reperfusion injury has been demonstrated. In this study, we aimed to investigate whether PDTC prevents harmful effects of superior mesenteric I/R injury in rats. Methods: Wistar-albino rats were randomly allocated into the following 4 groups: (1) sham-operated group-these animals underwent laparotomy without I/R injury (group I, n = 12); (2) sham+PDTC group-identical to sham-operated rats except for the administration of PDTC (100 mg/kg intravenous bolus) 30 minutes prior to the commencement of the experimental period (group II, n = 12); (3) I/R group-these animals underwent laparotomy and 60 minutes of ischemia followed by 120 minutes of reperfusion (group III, n = 12); (4) PDTC-treated group (100 mg/kg, intravenously, before the I/R, group IV, n = 12). All animals were killed, and intestinal tissue samples were obtained for investigation of intestinal mucosal injury, myeloperoxidase (MPO) activity, malondialdehyde (MDA) levels, glutathione (GSH) levels, and intestinal edema. Results: There was a statistically significant decrease in GSH levels, along with an increase in intestinal mucosal injury scores, MPO activity, MDA levels, and intestinal tissue wet-to-dry weight ratios in group III when compared to groups I, II, and IV (P < .05). However, PDTC treatment led to a statistically significant increase in GSH levels, along with a decrease in intestinal mucosal injury scores, MPO activity, MDA levels, and intestinal tissue wet-to-dry weight ratios in group IV (P < .05). Conclusions: This study showed that PDTC treatment significantly prevented the reperfusion injury caused by superior mesenteric I/R. Further clinical studies are needed to clarify whether PDTC may be a useful therapeutic agent to use in particular operations where the reperfusion injury occurs. © 2007 Excerpta Medica Inc. All rights reserved.

Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-27T11:21:21Z No. of bitstreams: 0Bitstream added on 2014-05-27T14:39:55Z : No. of bitstreams: 1 2-s2.0-23744472010.pdf: 529510 bytes, checksum: d4ae79c794c8b79242af56d545a4b4e6 (MD5) Made available in DSpace on 2014-05-27T11:21:21Z (GMT). No. of bitstreams: 0 Previous issue date: 2005-06-01 The intestinal ischemia is unusual in vascular surgery emergency. Its main causes are embolisms and arterial thrombosis. In addition to severe ischemia, reperfusion of the ischemic tissues can lead to several complications that may worsen the ischemic lesion and produce a life threatening situation caused by systemic alterations. Intestinal tissue injuries due to ischemia and reperfusion have been demonstrated in clinical and experimental studies, in which pathophysiology and adequate treatment were also studied. The great variety of experimental models used and results achieved reflect the need for an intestinal ischemia and reperfusion experimental model that is simple, reproducible and consistent, in order to search for treatments that can reduce the damage caused by this situation. In this review, the main pathophysiologic aspects and the most used experimental models will be reviewed. Copyright © 2005 by Sociedade Brasileira de Angiologia e Cirurgia Vascular. Aluno Regular do Curso de Pós-Graduação Nível Mestrado Universidade Estadual Paulista (UNESP), Botucatu, SP Livre-Docente da Disciplina de Cirurgia Vascular Departamento de Cirurgia e Ortopedia UNESP, Botucatu, SP Faculdade de Medicina de Botucatu Departamento de Cirurgia e Ortopedia, Botucatu, SP Aluno Regular do Curso de Pós-Graduação Nível Mestrado Universidade Estadual Paulista (UNESP), Botucatu, SP Livre-Docente da Disciplina de Cirurgia Vascular Departamento de Cirurgia e Ortopedia UNESP, Botucatu, SP Faculdade de Medicina de Botucatu Departamento de Cirurgia e Ortopedia, Botucatu, SP

The most important complication of intestinal malrotation is midgut volvulus because it may lead to intestinal ischaemia and necrosis. A 29-year-old male patient was admitted to the emergency department with abdominal pain. Ultrasonography (US), colour Doppler ultrasonography (CDUS), CT and barium studies were carried out. On US and CDUS, twisting of intestinal segments around the superior mesenteric artery (SMA) and superior mesenteric vein (SMV) and alteration of the SMA-SMV relationship were detected. CT demonstrated that the small intestine was making a rotation around the SMA and SMV, which amounted to more than 360°. The upper gastrointestinal barium series revealed a corkscrew appearance of the duodenum and proximal jejunum, which is a pathognomonic finding of midgut volvulus. Prior knowledge of characteristic imaging findings of midgut volvulus is essential in order to reach proper diagnosis and establish proper treatment before the development of intestinal ischaemia and necrosis. Copyright 2014 BMJ Publishing Group. All rights reserved.

We investigated the effect of antithrombin III on 60 min warm intestinal ischemia-reperfusion (IR) injury in rats. Sprague-Dawley rats, weighing 220-250 g, were divided into three groups: group 1 sham-operated group (no IR injury, n = 8), group 2 ischemic control group (control, Ringer's lactate infused, n = 8), group 3 Antithrombin III treated group (250 U/kg before ischemia, n = 8). Intestinal ischemia was induced in rats by occluding the superior mesenteric artery for 60 min. Malondialdehyde (MDA) levels, myeloperoxidase activity (MPO) and mucosal damage were investigated after 120 min reperfusion. Elevated MDA levels and MPO activity and severe histopathological damage were observed in the control group compared with the sham group (P < 0.05). Decreased MDA levels and MPO activity and less histopathological damage were detected in group 3 compared with the control group (P < 0.05). Accumulation of lipid peroxidation products and neutrophils in mucosal tissues were significantly inhibited by antithrombin III treatment. We conclude that treatment with antithrombin III before intestinal ischemia prevents histological damage in rats.