Although endometriosis is a disorder commonly found in reproductive-age women, it does not involve the bowel very often. The circumferential involvement of the rectum is rare and the obstructive symptoms can be difficult to differentiate from those of inflammatory or malignant diseases. We report two patients with rectal endometriosis whose first prominent symptoms were those of intestinal obstruction. A 26-year-old woman was admitted with obstructive symptoms. In order to alleviate the obstruction and extend the preoperative evaluation, a decompressive colostomy was done. The diagnosis of endometriosis was made by laparoscopy and biopsies of the thickened cul-de-sac peritoneum. Another woman, 40 years of age, was referred to us with a colostomy. She had undergone a laparotomy due to an obstructive acute abdomen a year before, and a frozen pelvis was found. Biopsy specimens had been collected and the pathological report revealed endometrioma. A rectosigmoidectomy, encompassing the stenotic rectal segment, was done along with primary anastomosis. The pathological examination confirmed rectal endometriosis. The conclusion is that, although rare, rectal endometriosis can cause significant stenosis of the organ, leading to obstructive symptoms. Despite its low frequency, it should always be considered in the differential diagnosis of rectal stenosis involving women of childbearing age.

Sepsis, the body's response to infection, is associated with extremely high mortality rates. Why a protective mechanism turns into a deadly clinical picture is a matter of debate, and goes largely unexplained. In previous work we demonstrated that platelet-derived microparticles (MP) can induce endothelial and vascular smooth muscle cell apoptosis in septic patients through NADPH oxidasedependent superoxide release [1]. In this work we sought to create a model for ex vivo generation of septic-like MP and to identify the pathways responsible for MP free radical release and effects. Septic shock is a condition related to the generation of high amounts of thrombin, TNFα and nitrogen reactive species. Human platelets exposed to the NO donors diethylamine-NONOate (0.5 mM) and nitroprusside (2 mM) for 20 minutes generated MP similar to those found in the blood of septic shock patients. Flow cytometry and western blot analysis of those MP, like their septic counterparts, revealed exposure of the tetraspanin markers CD9, CD63, and CD81, but little phosphatidylserine. Such a membrane exposure, associated with their size, characterizes them as exosomes. Furthermore, we identified the Nox2 and p22phox NADPH oxidase subunits and the inducible isoform of NO synthase (NOS), but not the NOS I and III isoforms. On the other hand, platelets exposed to thrombin or TNFα released particles with clearly distinct characteristics, such as high phosphatidylserine and low tetraspanin. Like the septic MP, the MP obtained by NO exposure generated the superoxide radical and NO, as disclosed by lucigenin (5 µM) and coelenterazine (5 µM) chemiluminescence and by 4,5-diaminofluorescein (10 mM) and 2′,7′-dichlorofluorescein (10 mM) fluorescence. As expected, NOS inhibitors or NADPH oxidase inhibitors significantly reduced signals. In addition, endothelial cells exposed to this type of MP underwent apoptotic death, while control MP had negligible effects. NADPH oxidase as well as NOS inhibition significantly reduced apoptosis rates. Concomitant generation of NO and superoxide suggests biological effects of the highly reactive radical peroxynitrite. In fact, the peroxynitrite scavenger urate (1 mM) showed an additive effect on fluorescent signal inhibition, as well as on endothelial apoptosis rate reduction. We thus propose that platelet-derived exosomes may be another class of actors in the complex play known as 'vascular redox signaling'. In this sense, an exosome-based approach can provide novel tools for further understanding and even treating vascular dysfunction related to sepsis. Introduction The intestinal hypothesis of sepsis has been attributed to bacterial translocation (BT), and the aggravation of sepsis is related to the increased vascular permeability state that potentates the BT index. In this study we examined the BT index during sepsis with or without mesenteric lymph exclusion. Materials and methods Wistar rats (±200 g) were submitted to the BT process (E. coli R6 10 ml of 10 10 CFU/ml) and nonlethal sepsis (E. cloacae 89 2 ml ...

Objectives To characterize an experimental model of pulmonary embolism by studying hemodynamics, lung mechanics and histopathologic derangements caused by pulmonary microembolism in pigs. To identify lung alterations after embolism that may be similar to those evidenced in pulmonary inflammatory conditions. Materials and methods Ten Large White pigs (weight 35-42 kg) were instrumented with arterial and pulmonary catheters, and pulmonary embolism was induced in five pigs by injection of polystyrene microspheres (diameter ~300 µM), in order to obtain a pulmonary mean arterial pressure of twice the baseline value. Five other animals injected with saline served as controls. Hemodynamic and respiratory data were collected and pressure x volume curves of the respiratory system were performed by a quasi-static low flow method. Animals were followed for 12 hours, and after death lung fragments were dissected and sent to pathology. Results Pulmonary embolism induced a significant reduction in stroke volume (71 ± 18 ml/min/bpm pre vs 36 ± 9 ml/min/bpm post, P < 0.05), an increase in pulmonary mean arterial pressure (27 ± 4 mmHg pre vs 39 ± 6 mmHg post, P < 0.05) and pulmonary vascular resistance (193 ± 122 mmHg/l/min pre vs 451 ± 149 mmHg/l/min post, P < 0.05). Respiratory dysfunction was evidenced by significant reductions in the PaO 2 /FiO 2 ratio (480 ± 50 pre vs 159 ± 55 post, P < 0.05), the dynamic lung compliance (27 ± 6 ml/cmH 2 O pre vs 19 ± 5 ml/cmH 2 O post, P < 0.05), the increase in dead space ventilation (20 ± 4 pre vs 47 ± 20 post, P < 0.05) and, the shift of pressure x volume curves to the right, with reduction in pulmonary hysteresis. Pathology depicted inflammatory neutrophil infiltrates, alveolar edema, collapse and hemorrhagic infarctions. Conclusion This model of embolism is associated with cardiovascular dysfunction, as well as respiratory injury characterized by a decrease in oxygenation, lung compliance and hysteresis. Pathology findings were similar to those verified in inflammatory pulmonary injury conditions. This model may be useful to study pathophysiology, as well as pharmacologic and ventilatory interventions useful to treat pulmonary embolism. P6 Hemodynamic and metabolic features of a porcine systemic low flow state model

Objectives To characterize an experimental model of pulmonary embolism by studying hemodynamics, lung mechanics and histopathologic derangements caused by pulmonary microembolism in pigs. To identify lung alterations after embolism that may be similar to those evidenced in pulmonary inflammatory conditions. Materials and methods Ten Large White pigs (weight 35-42 kg) were instrumented with arterial and pulmonary catheters, and pulmonary embolism was induced in five pigs by injection of polystyrene microspheres (diameter ~300 µM), in order to obtain a pulmonary mean arterial pressure of twice the baseline value. Five other animals injected with saline served as controls. Hemodynamic and respiratory data were collected and pressure x volume curves of the respiratory system were performed by a quasi-static low flow method. Animals were followed for 12 hours, and after death lung fragments were dissected and sent to pathology. Results Pulmonary embolism induced a significant reduction in stroke volume (71 ± 18 ml/min/bpm pre vs 36 ± 9 ml/min/bpm post, P < 0.05), an increase in pulmonary mean arterial pressure (27 ± 4 mmHg pre vs 39 ± 6 mmHg post, P < 0.05) and pulmonary vascular resistance (193 ± 122 mmHg/l/min pre vs 451 ± 149 mmHg/l/min post, P < 0.05). Respiratory dysfunction was evidenced by significant reductions in the PaO 2 /FiO 2 ratio (480 ± 50 pre vs 159 ± 55 post, P < 0.05), the dynamic lung compliance (27 ± 6 ml/cmH 2 O pre vs 19 ± 5 ml/cmH 2 O post, P < 0.05), the increase in dead space ventilation (20 ± 4 pre vs 47 ± 20 post, P < 0.05) and, the shift of pressure x volume curves to the right, with reduction in pulmonary hysteresis. Pathology depicted inflammatory neutrophil infiltrates, alveolar edema, collapse and hemorrhagic infarctions. Conclusion This model of embolism is associated with cardiovascular dysfunction, as well as respiratory injury characterized by a decrease in oxygenation, lung compliance and hysteresis. Pathology findings were similar to those verified in inflammatory pulmonary injury conditions. This model may be useful to study pathophysiology, as well as pharmacologic and ventilatory interventions useful to treat pulmonary embolism. P6 Hemodynamic and metabolic features of a porcine systemic low flow state model

Objectives To characterize an experimental model of pulmonary embolism by studying hemodynamics, lung mechanics and histopathologic derangements caused by pulmonary microembolism in pigs. To identify lung alterations after embolism that may be similar to those evidenced in pulmonary inflammatory conditions. Materials and methods Ten Large White pigs (weight 35-42 kg) were instrumented with arterial and pulmonary catheters, and pulmonary embolism was induced in five pigs by injection of polystyrene microspheres (diameter ~300 µM), in order to obtain a pulmonary mean arterial pressure of twice the baseline value. Five other animals injected with saline served as controls. Hemodynamic and respiratory data were collected and pressure x volume curves of the respiratory system were performed by a quasi-static low flow method. Animals were followed for 12 hours, and after death lung fragments were dissected and sent to pathology. Results Pulmonary embolism induced a significant reduction in stroke volume (71 ± 18 ml/min/bpm pre vs 36 ± 9 ml/min/bpm post, P < 0.05), an increase in pulmonary mean arterial pressure (27 ± 4 mmHg pre vs 39 ± 6 mmHg post, P < 0.05) and pulmonary vascular resistance (193 ± 122 mmHg/l/min pre vs 451 ± 149 mmHg/l/min post, P < 0.05). Respiratory dysfunction was evidenced by significant reductions in the PaO 2 /FiO 2 ratio (480 ± 50 pre vs 159 ± 55 post, P < 0.05), the dynamic lung compliance (27 ± 6 ml/cmH 2 O pre vs 19 ± 5 ml/cmH 2 O post, P < 0.05), the increase in dead space ventilation (20 ± 4 pre vs 47 ± 20 post, P < 0.05) and, the shift of pressure x volume curves to the right, with reduction in pulmonary hysteresis. Pathology depicted inflammatory neutrophil infiltrates, alveolar edema, collapse and hemorrhagic infarctions. Conclusion This model of embolism is associated with cardiovascular dysfunction, as well as respiratory injury characterized by a decrease in oxygenation, lung compliance and hysteresis. Pathology findings were similar to those verified in inflammatory pulmonary injury conditions. This model may be useful to study pathophysiology, as well as pharmacologic and ventilatory interventions useful to treat pulmonary embolism. P6 Hemodynamic and metabolic features of a porcine systemic low flow state model