976 resultados para aorta abdominal


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El manejo del trauma abdominal supone el reto de realizar una anastomosis o sutura intestinal en pacientes comprometidos hemodinámicamente. La decisión de cirugía de control de daños ante la presencia de acidosis, hipotermia y coagulopatía es evidente, sin embargo la situación no siempre es tan clara. En individuos con trauma se desarrollan cambios moleculares e inflamatorios por inadecuado balance entre aporte y demanda de oxígeno, que afectan el proceso de reparación de los tejidos con el riesgo de aparición de fístulas. Una forma rápida y práctica de detectar esta hipoperfusión es midiendo la saturación venosa de oxígeno (SVO2) y el Lactato Sérico. OBJETIVOS: Establecer correlación entre los valores de SVO2 transoperatorio y la aparición de fístulas intestinales en pacientes intervenidos por trauma abdominal. MATERIALES Y METODOS: Estudio de cohorte prospectivo que analiza diferentes variables en relación con la aparición de fistulas en pacientes con trauma abdominal que requieren suturas en el tracto gastrointestinal, haciendo énfasis en los niveles de SVO2. RESULTADOS: Los pacientes con falla anastomótica, presentaron un promedio de SVO2 más baja (60.0% ± 2.94%), versus los no fistulizados (69.89% ± 7.21%) (p =0.010). Todos los pacientes de la cohorte expuesta (SVO2<65%), presentaron dehiscencia de la anastomosis (RR =39.8, IC95%: 2.35,659.91, p<0.001, Test exacto de Fisher). El valor predictivo positivo de la saturación (<65%) fue de 57.14% (IC 95%: 13.34%, 100%) y el valor predictivo negativo fue de 100% (IC 95%:81.75%, 100%). La sensibilidad fue de 100% (IC 95%:87.50%, 100%) y especificidad de 91.89% (IC 95%: 81.75%, 100%). En el análisis bivariante determinó que el índice de trauma abdominal, el nivel de hemoglobina y el requerimiento de transfusión de glóbulos rojos, son factores de riesgo directamente relacionados con la falla de la anastomosis en pacientes con trauma abdominal CONCLUSIONES: - Hay una fuerte relación entre la falla en la reparación intestinal y SVO2 < 65%. - El pronóstico de una anastomosis intestinal está directamente relacionada con el estado hemodinámico y la perfusión tisular al momento de la intervención quirúrgica. - El nivel de SVO2 puede apoyar al cirujano en la decisión de realizar o no una reparación en víscera hueca al momento de intervención quirúrgica en un paciente con trauma abdominal.

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The abdominal compartment syndrome (ACS) is the result of various physiological alterations produced by an abnormal increase of the intra-abdominal pressure. Some of these patients will undergo a surgical procedure for its management. Methods: This is a retrospective case series of 28 patients with ACS who required surgical treatment at the Hospital Occidente de Kennedy between 1999 and 2003. We assessed retrospectively the behavior of McNelis’s equation for prediction of the development of the ACS. Results: The leading cause of ACS in our study was intraabadominal infection (n=6 21,4%). Time elapsed between diagnosis and surgical decompression was less than 4 hours in 75% (n=21) of the cases. The variables that improved significantly after the surgical decompression were CVP (T: 4,0 p: 0,0001), PIM (T: 2,7; p: 0,004), PIA (T1,8; p:0,034) and Urine Output (T:-2,4; p:0,02). The values of BUN, Creatinine and the cardiovascular instability did not show improvement. The ICU and hospital length of stay were 11 days (SD: 9) and 18 days (SD13) respectively. Global mortality was 67,9% (n=19) and mortality directly attributable to the syndrome was 30% (n=8). The behavior of the McNelis’s equation was erratic. Conclusions: The demographic characteristics as well as disease processes associated with ACS are consistent with the literature. The association between physiological variables and ACS is heterogeneous between patients. Mortality rates attributable to ACS in our institution are within the range described world-wide. The behavior of the McNelis’s equation seems to depend greatly upon fluid balance.

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Introducción: La evaluación de injertos vasculares de submucosa de intestino delgado para la regeneración de vasos sanguíneos ha producido una permeabilidad variable (0-100%) que ha sido concurrente con la variabilidad en las técnicas de fabricación. Metodología: Investigamos los efectos de fabricación en permeabilidad y regeneración en un diseño experimental de 22factorial que combino: 1) preservación (P) o remoción (R) de la capa estratum compactum del intestino, y 2) deshidratada (D) o hidratada (H), dentro de cuatro grupos de estudio (PD, RD, PH, RH). Los injertos fueron implantados en las Arterias Carótidas de porcinos (ID 4.5mm, N=4, 7d). Permeabilidad, trombogenicidad, reacción inflamatoria, vascularización, infiltración de fibroblastos, perfil de polarización de macrófagos y fuerza tensil biaxial fueron evaluadas. Resultados: Todos los injertos PD permanecieron permeables (4/4), pero tuvieron escasa vascularización e infiltración de fibroblastos. El grupo RD permaneció permeable (4/4), presentó una extensa vascularización e infiltración de fibroblastos, y el mayor número del fenotipo de macrófagos (M2) asociado a regeneración. El grupo RH presentó menor permeabilidad (3/4), una extensa vascularización e infiltración de fibroblastos, y un perfil dominante de M2. El grupo PH presentó el menor grado de permeabilidad, y a pesar de mayor infiltración celular que PD, exhibió un fenotipo de macrófagos dominante adverso. La elasticidad de los injertos R evolucionó de una manera similar a las Carótidas nativas (particularmente RD, mientras que los injertos P mantuvieron su rigidez inicial. Discusión: Concluimos que los parámetros de fabricación afectan drásticamente los resultados, siendo los injertos RD los que arrojaron mejores resultados.

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Introdução: O precondicionamento isquêmico é o mais poderoso método experimental de proteção celular e pode ser aplicado em cirurgias que ocasionem isquemia tecidual como na correção de coarctação da aorta. Objetivo: Avaliar os resultados clínicos, inflamatórios e infecciosos de crianças submetidas à cirurgia de coarctação da aorta com ou sem uso de precondicionamento isquêmico por pinçamento da aorta torácica. Como desfechos primários foram avaliados os Eventos Adversos Principais (EAP) e o óbito em até 30 dias. Método: Foram analisados retrospectivamente os dados clínicos de 104 pacientes submetidos consecutivamente a cirurgia de coarctação da aorta entre dezembro de 2007 e dezembro de 2012 no Instituto Nacional de Cardiologia, Centro Pediátrico da Lagoa e Hospital Prontobaby na cidade do Rio de Janeiro. Foram constituídos dois grupos, G PRE: 27 pacientes submetidos ao precondicionamento e G CONT: 77 pacientes de controle Resultados: Houve predomínio do sexo masculino, 62,5%, a média de peso foi de 4,04±3,07 kg e 11,53% tinham peso < 2,5kg. A média de idade foi de 3,82±2, com mediana de 1,04 meses. A cirurgia foi realizada em caráter de emergência em 81,48% no G PRE (p<0,001) e o Basic e o Comprehensive Aristotle Score foram maiores no G CONT (p<0,001). A bandagem da artéria pulmonar foi realizada em 37,9% do G PRE contra 9,09% do G CONT e 81,48% do G PRE tiveram anastomose estendida no arco aórtico (p<0,001). As complicações aconteceram em 66,23% no G CONT e em 22,22% no G PRE (p<0,001). Os tempos de entubação traqueal, internação no CTI e internação hospitalar do G CONT foram 3 vezes (p=0,281), 2,44 vezes (p=0,175) e 1,7 vezes (p=0,196) maior que do G PRE. Os EAP aconteceram somente no G CONT (p>0,05), sendo mais comuns os abdominais (8,65%). Ocorreram três óbitos cirúrgicos (2,88%) todos no Grupo CONT (3,90%) (p=0,401). Nove pacientes (8,65%) tiveram óbito na internação da cirurgia, um do G PRE (3,70%) e oito do G CONT (10,39%) (p=0,265). As curvas livres de desfecho em 30 dias (100%) e 60 meses (74,07%) foram favoráveis para o Grupo PRE (p=0,007 e p=0,017). A análise multivariada de COX demonstrou que as variáveis: cateterismo venoso prévio, interrupção de arco aórtico, ventrículo único, hipertensão arterial pulmonar e a dupla via de saída de VD estão associados ao aumento de risco para desfecho nos pacientes do G PRE (p<0,05). Conclusão: Os pacientes do G PRE apresentaram maior complexidade e risco operatório e menores índices de complicação. Os desfechos foram mais comuns no G CONT mesmo sem diferença estatística. A evolução livre de desfecho com 30 dias e até 60 meses foi favorável para o G PRE. A análise multivariada revelou grupo de variáveis em que o pré- condicionamento é desfavorável para aparecimento de desfecho em 30 dias

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BACKGROUND & AIMS: The mechanisms underlying abdominal pain perception in irritable bowel syndrome (IBS) are poorly understood. Intestinal mast cell infiltration may perturb nerve function leading to symptom perception. We assessed colonic mast cell infiltration, mediator release, and spatial interactions with mucosal innervation and their correlation with abdominal pain in IBS patients. METHODS: IBS patients were diagnosed according to Rome II criteria and abdominal pain quantified according to a validated questionnaire. Colonic mucosal mast cells were identified immunohistochemically and quantified with a computer-assisted counting method. Mast cell tryptase and histamine release were analyzed immunoenzymatically. Intestinal nerve to mast cell distance was assessed with electron microscopy. RESULTS: Thirty-four out of 44 IBS patients (77%) showed an increased area of mucosa occupied by mast cells as compared with controls (9.2% +/- 2.5% vs. 3.3 +/- 0.8%, respectively; P < 0.001). There was a 150% increase in the number of degranulating mast cells (4.76 +/- 3.18/field vs. 2.42 +/- 2.26/field, respectively; P = 0.026). Mucosal content of tryptase was increased in IBS and mast cells spontaneously released more tryptase (3.22 +/- 3.48 pmol/min/mg vs. 0.87 +/- 0.65 pmol/min/mg, respectively; P = 0.015) and histamine (339.7 +/- 59.0 ng/g vs. 169.3 +/- 130.6 ng/g, respectively; P = 0.015). Mast cells located within 5 microm of nerve fibers were 7.14 +/- 3.87/field vs. 2.27 +/- 1.63/field in IBS vs. controls (P < 0.001). Only mast cells in close proximity to nerves were significantly correlated with severity and frequency of abdominal pain/discomfort (P < 0.001 and P = 0.003, respectively). CONCLUSIONS: Colonic mast cell infiltration and mediator release in proximity to mucosal innervation may contribute to abdominal pain perception in IBS patients.

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OBJECTIVE: The objective of the study was to examine body fat distribution using computed tomography (CT), dual-energy X-ray absorptiometry (DEXA), and anthropometry in relation to type 2 diabetes in urban Asian Indians. RESEARCH DESIGN AND METHODS: This is a case-control study of 82 type 2 diabetic and 82 age- and sex-matched nondiabetic subjects from the Chennai Urban Rural Epidemiology Study, an ongoing epidemiological study in southern India. Visceral, subcutaneous, and total abdominal fat were measured using CT, while DEXA was used to measure central abdominal and total body fat. Anthropometric measures included BMI, waist circumference, sagittal abdominal diameter (SAD), and waist-to-hip ratio. RESULTS: Visceral and central abdominal fat showed a strong correlation with each other (P <0.0001), and kappa analysis revealed a fairly good agreement between tertiles of visceral and central abdominal fat (kappa=0.44, P <0.0001). Diabetic subjects had significantly higher visceral (P=0.005) and central abdominal (P=0.011) fat compared with nondiabetic subjects. Waist circumference and SAD showed a strong correlation with visceral (P <0.01) and central abdominal (P <0.0001) fat in both diabetic and nondiabetic subjects. Logistic regression analysis revealed visceral (odds ratio [OR] 1.011, P=0.004) and central abdominal (OR 1.001, P=0.013) fat to be associated with diabetes, even after adjusting for age and sex. CONCLUSIONS: Visceral and central abdominal fat showed a strong association with type 2 diabetes. Both measures correlated well with each other and with waist circumference and SAD in diabetic and nondiabetic urban Asian Indians.

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Ogihara CA, Schoorlemmer GHM, Levada AC, Pithon-Curi TC, Curi R, Lopes OU, Colombari E, Sato MA. Exercise changes regional vascular control by commissural NTS in spontaneously hypertensive rats. Am J Physiol Regul Integr Comp Physiol 299: R291-R297, 2010. First published April 21, 2010; doi: 10.1152/ajpregu.00055.2009.-Inhibition of the commissural nucleus of the solitary tract (commNTS) induces a fall in sympathetic nerve activity and blood pressure in spontaneously hypertensive rats (SHR), which suggests that this subnucleus of the NTS is a source of sympathoexcitation. Exercise training reduces sympathetic activity and arterial pressure. The purpose of the present study was to investigate whether the swimming exercise can modify the regional vascular responses evoked by inhibition of the commNTS neurons in SHR and normotensive Wistar-Kyoto (WKY) rats. Exercise consisted of swimming, 1 h/day, 5 days/wk for 6 wks, with a load of 2% of the body weight. The day after the last exercise session, the rats were anesthetized with intravenous alpha-chloralose, tracheostomized, and artificially ventilated. The femoral artery was cannulated for mean arterial pressure (MAP) and heart rate recordings, and Doppler flow probes were placed around the lower abdominal aorta and superior mesenteric artery. Microinjection of 50 mM GABA into the commNTS caused similar reductions in MAP in swimming and sedentary SHR (-25 +/- 6 and -30 +/- 5 mmHg, respectively), but hindlimb vascular conductance increased twofold in exercised vs. sedentary SHR (54 +/- 8 vs. 24 +/- 5%). GABA into the commNTS caused smaller reductions in MAP in swimming and sedentary WKY rats (-20 +/- 4 and -16 +/- 2 mmHg). Hindlimb conductance increased fourfold in exercised vs. sedentary WKY rats (75 +/- 2% vs. 19 +/- 3%). Therefore, our data suggest that the swimming exercise induced changes in commNTS neurons, as shown by a greater enhancement of hindlimb vasodilatation in WKY vs. SHR rats in response to GABAergic inhibition of these neurons.

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The aim of the present study was to evaluate the effect of overstimulation of beta-adrenoceptors on vascular inflammatory mediators. Wistar rats were treated with the beta-adrenoceptor agonist isoproterenol (0.3 mg(.)kg(-1.)day(-1) sc) or vehicle (control) for 7 days. At the end of treatment, the right carotid artery was catheterized for arterial and left ventricular (LV) hemodynamic evaluation. Isoproterenol treatment increased LV weight but did not change hemodynamic parameters. Aortic mRNA and protein expression were quantified by real-time RT-PCR and Western blot analysis, respectively. Isoproterenol enhanced aortic mRNA and protein expression of IL-1 beta (124% and 125%) and IL-6 (231% and 40%) compared with controls but did not change TNF-alpha expression. The nuclear-to-cytoplasmatic protein expression ration of the NF-beta B p65 subunit was increased by isoproterenol treatment (51%); in addition, it reduced the cytoplasmatic expression of I kappa B-alpha (52%) in aortas. An electrophoretic mobility shift assay was performed using the aorta, and increased NF-kappa B DNA binding (31%) was observed in isoproterenol-treated rats compared with controls (P < 0.05). Isoproterenol treatment increased phenylephrine-induced contraction in aortic rigs (P < 0.05), which was significantly reduced by superoxide dismutase (150 U/ml) and sodium salicylate (5 mM). Cotreatment with thalidomide (150 mg(.)kg(-1.)day(-1) for 7 days) also reduced hyperreactivity to phenylephrine induced by isoproterenol. In conclusion, overstimulation of beta-adrenoceptors increased proinflammatory cytokines and upregulated NF-kappa B in the rat aorta. Moreover, local oxidative stress and the proinflammatory state seem to play key roles in the altered vascular reactivity of the rat aorta induced by chronic beta-adrenergic stimulation.

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Disturbances in the regulation of cytosolic calcium (Ca(2+)) concentration play a key role in the vascular dysfunction associated with arterial hypertension. Stromal interaction molecules (STIMs) and Orai proteins represent a novel mechanism to control store-operated Ca(2+) entry. Although STIMs act as Ca(2+) sensors for the intracellular Ca(2+) stores, Orai is the putative pore-forming component of Ca(2+) release-activated Ca(2+) channels at the plasma membrane. We hypothesized that augmented activation of Ca(2+) release-activated Ca(2+)/Orai-1, through enhanced activity of STIM-1, plays a role in increased basal tonus and vascular reactivity in hypertensive animals. Endothelium-denuded aortic rings from Wistar-Kyoto and stroke-prone spontaneously hypertensive rats were used to evaluate contractions because of Ca(2+) influx. Depletion of intracellular Ca(2+) stores, which induces Ca(2+) release-activated Ca(2+) activation, was performed by placing arteries in Ca(2+) free-EGTA buffer. The addition of the Ca(2+) regular buffer produced greater contractions in aortas from stroke-prone spontaneously hypertensive rats versus Wistar-Kyoto rats. Thapsigargin (10 mu mol/L), an inhibitor of the sarcoplasmic reticulum Ca(2+) ATPase, further increased these contractions, especially in stroke-prone spontaneously hypertensive rat aorta. Addition of the Ca(2+) release-activated Ca(2+) channel inhibitors 2-aminoethoxydiphenyl borate (100 mu mol/L) or gadolinium (100 mu mol/L), as well as neutralizing antibodies to STIM-1 or Orai-1, abolished thapsigargin-increased contraction and the differences in spontaneous tone between the groups. Expression of Orai-1 and STIM-1 proteins was increased in aorta from stroke-prone spontaneously hypertensive rats when compared with Wistar-Kyoto rats. These results support the hypothesis that both Orai-1 and STIM-1 contribute to abnormal vascular function in hypertension. Augmented activation of STIM-1/Orai-1 may represent the mechanism that leads to impaired control of intracellular Ca(2+) levels in hypertension. (Hypertension. 2009; 53[part 2]: 409-416.)