Mesenteric venous thrombosis: MDCT features according to the underlying etiology [C-463]

Purpose: To work out certain, well‑defined aetiologies frequently associated with mesenteric venous thrombosis (MVT) in order to predict a typical population at risk, since MVT is nowadays often incidentally detected on cross‑sectional imaging. To demonstrate the MDCT features, frequency and extent of associated bowel ischemia according to the underlying pathology. Methods and Materials: Our electronic database revealed 71 patients (25 women, mean age 55) with thrombosis of the superior and/or inferior mesenteric vein detected by MDCT between 2000 and 2008. Two radiologists jointly reviewed the corresponding MDCT features including intraluminal extension, underlying aetiology and associated bowel ischemia, if present. Results: MVT was associated with carcinoma in 31 (43.7%) patients (pancreas 21.1%, liver 9.9%, others 12.7%). Concomitant inflammation was seen in 15 (21.1%) patients (pancreatitis 11.3%, diverticulitis 4.2%, others 5.6%), whereas coagulation/hematologic disorders were found in 7 (9.9%) patients, liver cirrhosis in 6 (8.5%), mixed/miscellaneous causes in 5 (7%) and still unknown aetiologies in 5 patients (7%). MVT resulted from recent operations in 2 (2.8%) patients. MDCT features of venous bowel ischemia were present in 15 patients (21.1%). 46.5% of MVT were (sub)acute, while 53.5% chronic. The luminal extension was complete in 52.1%, subtotal (50% of lumen) in 22.5% and partial (50% of lumen) in 25.4% of patients, consisting either of blood clots (76.1%) or tumoral tissue (23.9%), the latter mainly due to pancreas adenocarcinoma (76.4%). Conclusion: MDCT features of MVT are seen with a wide range of underlying diseases. Signs of intestinal ischemia are infrequently associated, mostly occurring with coagulation/hematologic disorders (40%).

Enteral nutrition and cardiovascular failure: from myths to clinical practice.

Cardiovascular failure and low flow states may arise in very different conditions from both cardiac and noncardiac causes. Systemic hemodynamic failure inevitably alters splanchnic blood flow but in an unpredictable way. Prolonged low splanchnic blood flow causes intestinal ischemia, increased mucosal permeability, endotoxemia, and distant organ failure. Mortality associated with intestinal ischemia is high. Why would enteral nutrition (EN) be desirable in these complex patients when parenteral nutrition could easily cover energy and substrate requirements? Metabolic, immune, and practical reasons justify the use of EN. In addition, continuous enteral feeding minimizes systemic and myocardial oxygen consumption in patients with congestive heart failure. Further, early feeding in critically ill mechanically ventilated patients has been shown to reduce mortality, particularly in the sickest patients. In a series of cardiac surgery patients with compromised hemodynamics, absorption has been maintained, and 1000-1200 kcal/d could be delivered by enteral feeding. Therefore, early EN in stabilized patients should be attempted, and can be carried out safely under close clinical monitoring, looking for signs of incipient intestinal ischemia. Energy delivery and balance should be monitored, and combined feeding considered when enteral feeds cannot be advanced to target within 4-6 days.

Mesenteric venous thrombosis : MDCT features according to the underlying etiology : P1

Purpose: To work out certain, well-defined aetiologies frequently associated with mesenteric venous thrombosis (MVT) in order to predict a typical population at risk, since MVT is nowadays often incidentally detected on cross-sectional imaging. To demonstrate the MDCT features, frequency and extent of associated bowel ischemia according to the underlying pathology. Methods and materials: Our electronic database revealed 71 patients (25 women, mean age 55) with thrombosis of the superior and/or inferior mesenteric vein detected by MDCT between 2000 and 2008. Two radiologists jointly reviewed the corresponding MDCT features including intraluminal extension, underlying aetiology and associated bowel ischemia, if present. Results: MVT was associated with carcinoma in 31 (43.7%) patients (pancreas 21.1%, liver 9.9%, others 12.7%). Concomitant inflammation was seen in 15 (21.1%) patients (pancreatitis 11.3%, diverticulitis 4.2%, others 5.6%), whereas coagulation/hematologic disorders were found in 7 (9.9%) patients, liver cirrhosis in 6 (8.5%), mixed/miscellaneous causes in 5 (7%) and still unknown aetiologies in 5 patients (7%). MVT resulted from recent operations in 2 (2.8%) patients. MDCT features of venous bowel ischemia were present in 15 patients (21.1%). 46.5% of MVT were (sub) acute, while 53.5% chronic. The luminal extension was complete in 52.1%, subtotal (>50% of lumen) in 22.5% and partial (<50% of lumen) in 25.4% of patients, consisting either of blood clots (76.1%) or tumoral tissue (23.9%), the latter mainly due to pancreas adenocarcinoma (76.4%). Conclusion: MDCT features of MVT are seen with a wide range of underlying diseases. Signs of intestinal ischemia are infrequently associated, mostly occurring with coagulation/hematologic disorders (40%).

Lesões intestinais decorrentes de isquemia e reperfusão: Fisiopatologia e modelos experimentais

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.

Aspectos clínicos-laboratoriais do uso do azul de metileno na obstrução experimental do jejuno em equinos expostos ao lipopolissacarídeo (LPS)

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Generation of in vivo activating factors in the ischemic intestine by pancreatic enzymes

One of the early events in physiological shock is the generation of activators for leukocytes, endothelial cells, and other cells in the cardiovascular system. The mechanism by which these activators are produced has remained unresolved. We examine here the hypothesis that pancreatic digestive enzymes in the ischemic intestine may be involved in the generation of activators during intestinal ischemia. The lumen of the small intestine of rats was continuously perfused with saline containing a broadly acting pancreatic enzyme inhibitor (6-amidino-2-naphthyl p-guanidinobenzoate dimethanesulfate, 0.37 mM) before and during ischemia of the small intestine by splanchnic artery occlusion. This procedure inhibited activation of circulating leukocytes during occlusion and reperfusion. It also prevented the appearance of activators in portal venous and systemic artery plasma and attenuated initiating symptoms of multiple organ injury in shock. Intestinal tissue produces only low levels of activators in the absence of pancreatic enzymes, whereas in the presence of enzymes, activators are produced in a concentration- and time-dependent fashion. The results indicate that pancreatic digestive enzymes in the ischemic intestine serve as an important source for cell activation and inflammation, as well as multiple organ failure.

Ischemic post-conditioning attenuates the intestinal injury induced by limb ischemia/reperfusion in rats

The purpose of this study was to investigate the protective effects of ischemic post-conditioning on damage to the barrier function of the small intestine caused by limb ischemia-reperfusion injury. Male Wistar rats were randomly divided into 3 groups (N = 36 each): sham operated (group S), lower limb ischemia-reperfusion (group LIR), and post-conditioning (group PC). Each group was divided into subgroups (N = 6) according to reperfusion time: immediate (0 h; T1), 1 h (T2), 3 h (T3), 6 h (T4), 12 h (T5), and 24 h (T6). In the PC group, 3 cycles of reperfusion followed by ischemia (each lasting 30 s) were applied immediately. At all reperfusion times (T1-T6), diamine oxidase (DAO), superoxide dismutase (SOD), and myeloperoxidase (MPO) activity, malondialdehyde (MDA) intestinal tissue concentrations, plasma endotoxin concentrations, and serum DAO, tumor necrosis factor-α (TNF-α), and interleukin-10 (IL-10) concentrations were measured in sacrificed rats. Chiu’s pathology scores for small intestinal mucosa were determined under a light microscope and showed that damage to the small intestinal mucosa was lower in group PC than in group LIR. In group PC, tissue DAO and SOD concentrations at T2 to T6, and IL-10 concentrations at T2 to T5 were higher than in group LIR (P < 0.05); however, tissue MPO and MDA concentrations, and serum DAO and plasma endotoxin concentrations at T2 to T6, as well as TNF-α at T2 and T4 decreased significantly (P < 0.05). These results show that ischemic post-conditioning attenuated the permeability of the small intestines after limb ischemia-reperfusion injury. The protective mechanism of ischemic post-conditioning may be related to inhibition of oxygen free radicals and inflammatory cytokines that cause organ damage.

Intestinal intraluminal injection of glutamine increases trolox total equivalent antioxidant capacity (TEAC) in hepatic ischemia-reperfusion

OBJETIVO: Avaliar em um modelo experimental de isquemia-reperfusão hepática os efeitos da injeção intraluminal de glutamina na capacidade anti-oxidante total em equivalência ao trolox (TEAC) do plasma, verificando a aplicabilidade de modificações ao método original de dosagem. MÉTODOS: Trinta ratos Wistar foram submetidos a laparotomia e confecção de uma alça fechada de 20 cm de comprimento envolvendo o intestinal delgado distal seguido do clampeamento do hilo hepático por 30 minutos e reperfusão por 5 minutos. Na alça fechada foi injetada glutamina (grupo glutamina; n=10) ou água destilada (grupo controle; n=10). Em dez animais (grupo sham) não foi realizado clampeamento hilar. Coletou-se sangue para dosagem da capacidade antioxidante total em equivalência ao trolox em condições modificadas de temperatura, proporções relativas dos reagentes e tempo de leitura sob espectrofotometria. RESULTADOS: A capacidade antioxidante total foi significantemente maior (p<0.05) no grupo glutamina que no grupo controle (1,60[1,55-1,77] vs 1,44[1,27-1,53]) e grupo sham (1,60[1,55-1,77] vs 1,48[1,45-1,59]). Não houve diferenças estatísticas entre o grupo controle e o grupo sham. CONCLUSÃO: A glutamina melhorou a capacidade anti-oxidante total plasmática. O método de dosagem refletiu consistentemente alterações na defesa anti-oxidante nesse modelo experimental.

Gut Bacteria Products Prevent Aki Induced By Ischemia-reperfusion.

Short-chain fatty acids (SCFAs) are fermentation end products produced by the intestinal microbiota and have anti-inflammatory and histone deacetylase-inhibiting properties. Recently, a dual relationship between the intestine and kidneys has been unraveled. Therefore, we evaluated the role of SCFA in an AKI model in which the inflammatory process has a detrimental role. We observed that therapy with the three main SCFAs (acetate, propionate, and butyrate) improved renal dysfunction caused by injury. This protection was associated with low levels of local and systemic inflammation, oxidative cellular stress, cell infiltration/activation, and apoptosis. However, it was also associated with an increase in autophagy. Moreover, SCFAs inhibited histone deacetylase activity and modulated the expression levels of enzymes involved in chromatin modification. In vitro analyses showed that SCFAs modulated the inflammatory process, decreasing the maturation of dendritic cells and inhibiting the capacity of these cells to induce CD4(+) and CD8(+) T cell proliferation. Furthermore, SCFAs ameliorated the effects of hypoxia in kidney epithelial cells by improving mitochondrial biogenesis. Notably, mice treated with acetate-producing bacteria also had better outcomes after AKI. Thus, we demonstrate that SCFAs improve organ function and viability after an injury through modulation of the inflammatory process, most likely via epigenetic modification.

The role of interleukin-6, endothelins, and apoptotic genes in small bowel transplantation, in a swine model of ischemia and reperfusion injury

IRI is closely related to sepsis in ITx setting. Complete understanding of the mechanisms involved in IRI development may improve outcomes. Ortothopic ITx without immunosuppression was performed in order to characterize IRI-associated mucosal damage. Twenty pigs underwent ITx. Two groups were assigned to different CI times: G1: 90 min and, G2: 180 min. Euro-Collins was used as preservation solution. Jejunal fragments were collected at donor laparotomy, 30 min, and 3 days after reperfusion. IRI assessment involved: histopathologic analysis, quantification of MPO-positive cells through immunohistochemical studies, quantification of epithelial apoptotic cells using TUNEL staining, and quantification of IL-6, ET-1, Bak, and Bcl-XL genes expression by RT-PCR. Neutrophilic infiltration increased in a similar fashion in both groups, but lasted longer in G2. Apoptosis detected by TUNEL staining increased and anti-apoptotic gene Bcl-XL expression decreased significantly in G1, 3 days after surgery. Endothelin-1 and IL-6 genes expression increased 30 min after the procedure and returned to baseline 3 days after surgery. In conclusion, IL-6 and ET-1 are involved precociously in the development of intestinal IRI. Apoptosis was more frequently detected in G1 grafts by TUNEL-staining and by RT-PCR.

Enhanced-reality video fluorescence: a real-time assessment of intestinal viability.

OBJECTIVE: Our aim was to evaluate a fluorescence-based enhanced-reality system to assess intestinal viability in a laparoscopic mesenteric ischemia model. MATERIALS AND METHODS: A small bowel loop was exposed, and 3 to 4 mesenteric vessels were clipped in 6 pigs. Indocyanine green (ICG) was administered intravenously 15 minutes later. The bowel was illuminated with an incoherent light source laparoscope (D-light-P, KarlStorz). The ICG fluorescence signal was analyzed with Ad Hoc imaging software (VR-RENDER), which provides a digital perfusion cartography that was superimposed to the intraoperative laparoscopic image [augmented reality (AR) synthesis]. Five regions of interest (ROIs) were marked under AR guidance (1, 2a-2b, 3a-3b corresponding to the ischemic, marginal, and vascularized zones, respectively). One hour later, capillary blood samples were obtained by puncturing the bowel serosa at the identified ROIs and lactates were measured using the EDGE analyzer. A surgical biopsy of each intestinal ROI was sent for mitochondrial respiratory rate assessment and for metabolites quantification. RESULTS: Mean capillary lactate levels were 3.98 (SD = 1.91) versus 1.05 (SD = 0.46) versus 0.74 (SD = 0.34) mmol/L at ROI 1 versus 2a-2b (P = 0.0001) versus 3a-3b (P = 0.0001), respectively. Mean maximal mitochondrial respiratory rate was 104.4 (±21.58) pmolO2/second/mg at the ROI 1 versus 191.1 ± 14.48 (2b, P = 0.03) versus 180.4 ± 16.71 (3a, P = 0.02) versus 199.2 ± 25.21 (3b, P = 0.02). Alanine, choline, ethanolamine, glucose, lactate, myoinositol, phosphocholine, sylloinositol, and valine showed statistically significant different concentrations between ischemic and nonischemic segments. CONCLUSIONS: Fluorescence-based AR may effectively detect the boundary between the ischemic and the vascularized zones in this experimental model.

Hérnia de Littré causando obstrução intestinal

The authors describe a case of a 60-year-old male with a history of a mass and pain at the right inguinal and epigastric areas. He also reported symptoms of bowel obstruction. Physical examination revealed a mass at right inguinal area, which was not reducible or pulsatile. Surgical findings included hernial sac contents with loop of ileum with signs of ischemia and a Meckel's diverticulum. Histopathological examination showed herniation of the Meckel diverticulum -Littré hernia. The article discusses the history and the incidence of this rare form of hernia.

Effects of Ischemia and Reperfusion on P2X(2) Receptor Expressing Neurons of the Rat Ileum Enteric Nervous System

Purpose We investigated the effects of ischemia/reperfusion in the intestine (I/R-i) on purine receptor P2X(2)-immunoreactive (IR) neurons of the rat ileum. Methods The superior mesenteric artery was occluded for 45 min with an atraumatic vascular clamp and animals were sacrificed 4 h later. Neurons of the myenteric and submucosal plexuses were evaluated for immunoreactivity against the P2X(2) receptor, nitric oxide synthase (NOS), choline acetyl transferase (ChAT), calbindin, and calretinin. Results Following I/R-i, we observed a decrease in P2X(2) receptor immunoreactivity in the cytoplasm and surface membranes of neurons of the myenteric and submucosal plexuses. These studies also revealed an absence of calbindin-positive neurons in the I/R-i group. In addition, the colocalization of the P2X(2) receptor with NOS, ChAT, and calretinin immunoreactivity in the myenteric plexus was decreased following I/R-i. Likewise, the colocalization between P2X(2) and calretinin in neurons of the submucosal plexus was also reduced. In the I/R-i group, there was a 55.8% decrease in the density of neurons immunoreactive (IR) for the P2X(2) receptor, a 26.4% reduction in NOS-IR neuron, a 25% reduction in ChAT-IR neuron, and a 47% reduction in calretinin-IR neuron. The density of P2X(2) receptor and calretinin-IR neurons also decreased in the submucosal plexus of the I/R-i group. In the myenteric plexus, P2X(2)-IR, NOS-IR, ChAT-IR and calretinin-IR neurons were reduced in size by 50%, 49.7%, 42%, and 33%, respectively, in the I/R-i group; in the submucosal plexus, P2X(2)-IR and calretinin-IR neurons were reduced in size by 56% and 72.6%, respectively. Conclusions These data demonstrate that ischemia/reperfusion of the intestine affects the expression of the P2X(2) receptor in neurons of the myenteric and submucosal plexus, as well as density and size of neurons in this population. Our findings indicate that I/R-i induces changes in P2X(2)-IR enteric neurons that could result in alterations in intestinal motility.

Prevention of bacterial translocation using β-(1-3)-D-glucan in small bowel ischemia and reperfusion in rats

To investigate the role of β-(1-3)-D-glucan on 99mTc labelled Escherichia coli translocation and cytokines secretion in rats submitted to small bowel ischemia/reperfusion injury. Methods: Five groups (n=10 each) of Wistar rats were subjected to control(C), sham(S), group IR subjected to 45 min of bowel ischemia/60 min of reperfusion(I/R), and group I/R+glucan subjected to 45 min of bowel ischemia/60 min of reperfusion(I/R) and injected with 2mg/Kg intramuscular. Translocation of labelled bacteria to mesenteric lymph nodes, liver, spleen, lung and serum was determined using radioactivity/count and colony forming units/g(CFU/g). Serum TNFα, IL-1β, IL-6, IL-10 were measured by ELISA. Results: CFU/g and radioactivity/count were higher in I/R than in I/R+glucan rats. In C, S and S+glucan groups, bacteria and radioactivity/count were rarely detected. The I/R+glucan rats had enhancement of IL-10 and suppressed production of serum TNFα, IL-1β and, IL-6, compared to I/R untreated animals. Conclusion: The β-(1-3)-D-glucan modulated the production of pro-inflammatory and anti-inflammatory cytokines during bowel ischemia/reperfusion, and attenuated translocation of labelled bacteria

Prevention of bacterial translocation using β-(1-3)-D-glucan in small bowel ischemia and reperfusion in rats

To investigate the role of β-(1-3)-D-glucan on 99mTc labelled Escherichia coli translocation and cytokines secretion in rats submitted to small bowel ischemia/reperfusion injury. Methods: Five groups (n=10 each) of Wistar rats were subjected to control(C), sham(S), group IR subjected to 45 min of bowel ischemia/60 min of reperfusion(I/R), and group I/R+glucan subjected to 45 min of bowel ischemia/60 min of reperfusion(I/R) and injected with 2mg/Kg intramuscular. Translocation of labelled bacteria to mesenteric lymph nodes, liver, spleen, lung and serum was determined using radioactivity/count and colony forming units/g(CFU/g). Serum TNFα, IL-1β, IL-6, IL-10 were measured by ELISA. Results: CFU/g and radioactivity/count were higher in I/R than in I/R+glucan rats. In C, S and S+glucan groups, bacteria and radioactivity/count were rarely detected. The I/R+glucan rats had enhancement of IL-10 and suppressed production of serum TNFα, IL-1β and, IL-6, compared to I/R untreated animals. Conclusion: The β-(1-3)-D-glucan modulated the production of pro-inflammatory and anti-inflammatory cytokines during bowel ischemia/reperfusion, and attenuated translocation of labelled bacteria