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A thyroglossal duct cyst (TGDC) is the result of incomplete degeneration of the thyroglossal duct during gestation. It is the most common type of congenital cyst of the neck, and is usually seen in children. The tumor mostly appears at the midline of the neck and generally causes no symptoms, but the mass typically moves when the patient swallows. We present the unusual case of a 50-year-old man with a large cervical mass lateralized on the right side of the neck. There was no association between swallowing and movement of the mass. Clinical examination and computed tomography (CT) suggested a lymphangioma or cystic hygroma. Surgical resection showed a large cyst of 71 x 40 x 52 mm with no attachment to the hyoid bone and no invasion in blood vessels or other surrounding tissue. Histopathological investigation led to a diagnosis of TGDC.
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BACKGROUND: Temporal arteritis or giant cell arteritis is a form of systemic inflammatory vasculitis closely associated with polymyalgia rheumatica. It may have serious systemic, neurologic, and ophthalmic consequences as it may lead to impaired vision and blindness. Definitive diagnosis is made after histopathologic analysis of a superficial temporal artery (TA) biopsy, which requires a small surgical procedure often under local anesthesia. We investigated whether a noninvasive technique such as duplex ultrasound of the TA could replace histopathological analysis. METHODS: Eighty-one patients referred to our department for TA biopsy were first screened with a duplex ultrasound for a surrounding halo and/or occlusion of the TA. Presence of visual disturbances and unilateral pain (headache and/or tongue/jaw claudication) was noted before TA biopsy. Pathological analysis was considered the gold standard. Correlation between duplex findings, symptoms, and pathology was determined by Spearman's Rho test. The predictive value of a halo and TA occlusion on duplex were determined by ROC curve analysis. RESULTS: A halo or TA occlusion was found in 16.0% and 3.7% of patients, respectively. Unilateral pain was reported in 96% of cases while 82% complained of visual disturbances. Correlation coefficients for halo and occlusion were 0.471 and 0.404, respectively (P < 0.0001), suggesting a moderate correlation between duplex and biopsy. There was no significant correlation between visual impairment or pain and histologic findings. The ROC curve analysis showed a sensitivity of 53.3% and 20.0%, and specificity of 91.9% and 100% for presence of a halo and occlusion of the TA on duplex, respectively. CONCLUSIONS: Arterial duplex is a moderately sensitive but highly specific test for exclusion of temporal arteritis. We observed a moderate correlation between these findings on duplex and histopathological analysis as a gold standard. Arterial duplex may serve as a valuable diagnostic addition to prevent unnecessary surgical procedures and can even substitute biopsy in patients where surgery is not an option.
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Arteritis de Células Gigantes/diagnóstico por imagen , Arterias Temporales/diagnóstico por imagen , Ultrasonografía Doppler Dúplex , Adulto , Anciano , Anciano de 80 o más Años , Biopsia , Femenino , Arteritis de Células Gigantes/patología , Humanos , Masculino , Persona de Mediana Edad , Estudios Prospectivos , Sensibilidad y Especificidad , Arterias Temporales/patologíaRESUMEN
BACKGROUND: Pre-eclampsia (PE) is related to an impaired endothelial function. Endothelial dysfunction accounts for altered vascular reactivity, activation of the coagulation cascade and loss of vascular integrity. Impaired endothelial function originates from production of inflammatory and cytotoxic factors by the ischemic placenta and results in systemic oxidative stress (OS) and an altered bioavailability of nitric oxide (â¢NO). The free radical â¢NO, is an endogenous endothelium-derived relaxing factor influencing endothelial function. In placental circulation, endothelial release of â¢NO dilates the fetal placental vascular bed, ensuring feto-maternal exchange. The Endopreg study was designed to evaluate in vivo endothelial function and to quantify in vitro OS in normal and pre-eclamptic pregnancies. METHODS/DESIGN: The study is divided into two arms, a prospective longitudinal study and a matched case control study. In the longitudinal study, pregnant patients ≥18 years old with a singleton pregnancy will be followed throughout pregnancy and until 6 months post-partum. In the case control study, cases with PE will be compared to matched normotensive pregnant women. Maternal blood concentration of superoxide (O2â¢) and placental concentration of â¢NO will be determined using EPR (electron paramagnetic resonance). Endothelial function and arterial stiffness will be evaluated using respectively Peripheral Arterial Tonometry (PAT), Flow-Mediated Dilatation (FMD) and applanation tonometry. Placental expression of eNOS (endothelial NOS) will be determined using immune-histochemical staining. Target recruitment will be 110 patients for the longitudinal study and 90 patients in the case-control study. DISCUSSION: The results of Endopreg will provide longitudinal information on in vivo endothelial function and in vitro OS during normal pregnancy and PE. Adoption of these vascular tests in clinical practice potentially predicts patients at risk to develop cardiovascular events later in life after PE pregnancies. â¢NO, O2â¢- and eNOS measurements provide further inside in the pathophysiology of PE. TRIAL REGISTRATION: This trial has been registered on clinicaltrials.gov. ClinicalTrials.gov Identifier: NCT02603913 . Registered October 2015.
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Endotelio Vascular , Óxido Nítrico , Placenta/metabolismo , Preeclampsia , Adulto , Enfermedades Cardiovasculares/diagnóstico , Enfermedades Cardiovasculares/prevención & control , Estudios de Casos y Controles , Espectroscopía de Resonancia por Spin del Electrón/métodos , Endotelio Vascular/metabolismo , Endotelio Vascular/fisiopatología , Femenino , Humanos , Estudios Longitudinales , Óxido Nítrico/análisis , Óxido Nítrico/metabolismo , Óxido Nítrico Sintasa de Tipo III/metabolismo , Estrés Oxidativo , Preeclampsia/sangre , Preeclampsia/metabolismo , Preeclampsia/patología , Embarazo , Pronóstico , Superóxidos/sangre , Rigidez VascularRESUMEN
BACKGROUND: Malignant pleural mesothelioma (MPM) is a rare but aggressive neoplasm that typically originates from the mesothelial surfaces of the pleural cavity. Exposure to asbestos is the principal etiological agent of MPM. The disease is characterized by difficult stage classification and limited consensus on therapeutic approach. We have evaluated the experience with MPM in the Antwerp University Hospital over the past 15 years. METHODS: A database was created with all patients diagnosed with or treated for a MPM between 2001 and 2015. A total of 101 patients were included on which different survival analyses were performed combined with a reproduction of demographic, clinical, histologic and therapeutic data, and these were compared to literature data. RESULTS: Vast majority of our 101 patients were male (80%) with a median age of 66 years at diagnosis with predominantly epitheloid histology (81%). Overall median survival was 18.3 months and overall 1-, 2- and 5-year survival rates were 68%, 37% and 7%, respectively. Kaplan-Meier analysis showed a non-significant difference in survival between the several best (b) TNM-stages (p = .356). A significant difference in survival was observed in patients undergoing surgery versus no surgery (p = .008), between the different histological types (p < .0001) and treatment with chemotherapy alone versus chemotherapy with surgery (p < .0001). Smoking at diagnosis and epitheloid histology have been identified as significant prognostic factors in the multivariate Cox regression model (HR 3.13 and 0.53, respectively). CONCLUSION: Descriptive and survival analysis of our patient database confirmed the limitations of the current staging system and were concordant with literature regarding MPM.
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Neoplasias Pulmonares/patología , Mesotelioma/patología , Adulto , Anciano , Anciano de 80 o más Años , Bélgica , Terapia Combinada , Femenino , Humanos , Neoplasias Pulmonares/mortalidad , Neoplasias Pulmonares/terapia , Masculino , Mesotelioma/mortalidad , Mesotelioma/terapia , Mesotelioma Maligno , Persona de Mediana Edad , Estadificación de Neoplasias , Estudios Retrospectivos , Tasa de SupervivenciaRESUMEN
BACKGROUND: Pulmonary ischemia-reperfusion injury (IRI) causes postoperative morbidity in patients undergoing lung transplantation, isolated lung perfusion, and cardiopulmonary bypass and may lead to potentially lethal pathologies such as respiratory shock. In-depth study of this pathology requires a reliable animal model. Mice are a popular species to develop experimental models because of their logistic advantages and the availability of knock outs. However, their small size warrants microsurgical techniques and a skilled surgeon. MATERIALS AND METHODS: We developed a murine model of pulmonary anoxic IRI through hilar clamping using adult female Swiss mice. After left thoracotomy, we expose the pulmonary hilum keeping the ribs and the muscles of back and forepaw intact. A microvascular clamp is placed over the entire hilum, occluding bronchus, pulmonary artery, and vein. RESULTS: Our model proved to be simple, reliable, and reproducible, showing minimal preoperative and postoperative mortality. Histopathologic analysis indicated all characteristic features of pulmonary IRI, such as an early recruitment of lymphocytes followed by neutrophil influx. CONCLUSIONS: This article presents a murine surgery model for pulmonary IRI based on a muscle-sparing thoracotomy. The minimal approach limits manipulation of lung tissue, minimizing mortality and non-IRI-induced injury.
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Lesión Pulmonar Aguda/etiología , Modelos Animales de Enfermedad , Daño por Reperfusión/etiología , Animales , Femenino , Ratones Endogámicos BALB C , Ratones Endogámicos C57BL , Microcirugia/métodosRESUMEN
Background: Trochanteric fractures are very common hip injuries often fixed with intramedullary nailing as the recommended treatment. Medial lag screw migration of the intramedullary nail system is an uncommon complication. The objective of this case report is to highlight the importance of optimal reduction in hip fractures and the need for a multidisciplinary approach with vascular assistance in intrapelvic lag screw migration. Case report and results: We collected 24 cases of intrapelvic migration of the lag screw in the latest literature. Here, we report the case of a 68-year-old patient with medial pelvic migration of the lag screw after minor trauma and its removal using peroperative simultaneous angiography. After removal of the osteosynthesis material, a revision to a total hip arthroplasty was performed. Conclusion/discussion: This is the first case demonstrating an endovascular assisted removal simultaneous with revision surgery. We suggest that a multidisciplinary approach is warranted in which the orthopedic surgeon is assisted by a vascular surgeon. An endovascular assisted open removal of the lag screw with conversion to a hip arthroplasty is considered a safe treatment.
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Pulmonary ossifications have often been regarded as rare, post-mortem findings without any clinical significance. We have investigated the occurrence of pulmonary ossifications in patients undergoing thoracic procedures, and how this may affect the differential diagnosis of solitary pulmonary nodules. In addition, we have performed a literature search on the occurrence and possible pathogenesis of these ossifications. From January 2008 until August 2019, we identified pulmonary ossifications in 34 patients who underwent elective pulmonary surgery. Pre-operative imaging was unable to differentiate these ossifications from solid tumors. A definitive diagnosis was made by an experienced pathologist (VS, ML). The PubMed database was researched in December 2019 with the search terms "pulmonary ossifications"; "heterotopic ossifications"; and "solitary pulmonary nodule". In total, 27 patients were male, with a mean age of 63 ± 12 years (age 41 to 82 on diagnosis). All lesions were identified on thoracic CT and marked for resection by a multidisciplinary team. A total of 17 patients were diagnosed with malignancy concurrent with ossifications. There was a clear predilection for the right lower lobe (12 cases, 35.3%) and most ossifications had a nodular form (70.6%). We could not identify a clear association with any other pathology, either cancerous or non-cancerous in origin. Oncologic or pulmonary comorbidities did not influence patient survival. Pulmonary ossifications are not as seldom as thought and are not just a curiosity finding by pathologists. These formations may be mistaken for a malignant space-occupying lesion, both pre-and perioperatively, as they are indistinguishable in imaging. We propose these ossifications as an underestimated addition to the differential diagnosis of a solitary pulmonary nodule.
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Lung ischemia-reperfusion injury remains one of the major complications after cardiac bypass surgery and lung transplantation. Due to its dual blood supply system and the availability of oxygen from alveolar ventilation, the pathogenetic mechanisms of ischemia-reperfusion injury in the lungs are more complicated than in other organs, where loss of blood flow automatically leads to hypoxia. In this review, an extensive overview is given of the molecular and cellular mechanisms that are involved in the pathogenesis of lung ischemia-reperfusion injury and the possible therapeutic strategies to reduce or prevent it. In addition, the roles of neutrophils, alveolar macrophages, cytokines, and chemokines, as well as the alterations in the cell-death related pathways, are described in detail.
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Enfermedades Pulmonares/fisiopatología , Daño por Reperfusión/fisiopatología , Animales , Puente Cardiopulmonar/efectos adversos , Humanos , Enfermedades Pulmonares/prevención & control , Enfermedades Pulmonares/terapia , Trasplante de Pulmón/efectos adversos , Modelos Animales , Flujo Sanguíneo Regional , Daño por Reperfusión/prevención & control , Daño por Reperfusión/terapiaRESUMEN
BACKGROUND: Up to 66% of patients show local pulmonary disease progression after pulmonary metastasectomy. Regional treatment with isolated lung perfusion (ILuP) may improve local control with minimal systemic adverse effects. The aims of this study were to evaluate local and distant control after ILuP, determine the effect on overall survival compared with historical controls, and confirm the safety and feasibility of ILuP. METHODS: A total of 107 patients with resectable pulmonary metastases of colorectal carcinoma, osteosarcoma, and soft-tissue sarcoma were included in a prospective phase II study of pulmonary metastasectomy combined with ILuP with 45 mg melphalan at 37°C. Local and distant control, overall survival, lung function, and 90-day mortality and morbidity were monitored. RESULTS: We report 0% mortality, low morbidity, and no long-term pulmonary toxicity. For colorectal carcinoma, median time to local pulmonary progression, median time to progression, and median survival time were 31, 14, and 78 months, respectively. Median time to local progression was not reached for sarcoma, whereas median time to progression and median survival time were 13 and 39 months, respectively. The 5-year disease-free rate and pulmonary progression-free rate were 26% and 44% for colorectal carcinoma and 29% and 63% for sarcoma, respectively. CONCLUSIONS: ILuP with melphalan combined with metastasectomy is feasible and safe. Compared with historical controls, favorable results were obtained in this phase II study for local control. Further evaluation of locoregional lung perfusion techniques with other chemotherapeutic drugs is warranted.
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Antineoplásicos Alquilantes/uso terapéutico , Neoplasias Pulmonares/secundario , Melfalán/uso terapéutico , Metastasectomía , Perfusión , Sarcoma/secundario , Adulto , Anciano , Neoplasias Óseas/patología , Neoplasias Colorrectales/patología , Terapia Combinada , Progresión de la Enfermedad , Femenino , Estudio Históricamente Controlado , Humanos , Neoplasias Pulmonares/tratamiento farmacológico , Neoplasias Pulmonares/cirugía , Masculino , Persona de Mediana Edad , Estudios Prospectivos , Sarcoma/tratamiento farmacológico , Sarcoma/cirugía , Análisis de SupervivenciaRESUMEN
BACKGROUND: Two clinically used strategies for ex vivo lung perfusion (EVLP) were compared in a porcine model with respect to lung function, metabolism, inflammatory response, oxidative stress, and cell viability. METHODS: Porcine lungs (n = 20) were preserved, harvested, and kept cooled for 2 hours. After randomization, EVLP was performed using a cellular perfusate and open left atrium (COA group) or an acellular perfusate and a closed left atrium (ACA group). Oxygenation (partial pressure of arterial oxygen/fraction of inspired oxygen), compliance, dead space, weight, and perfusate oncotic pressure were registered before and after a 4-hour period of reconditioning. Lung tissue samples were collected before and after EVLP for quantitative polymerase chain reaction analysis of gene expression for inflammatory markers, measurement of tissue hypoxia (hypoxia inducible factor-1α) and oxidative stress (ascorbyl radical), and viability (trypan blue staining) and lung histopathology. RESULTS: In 3 of 10 lungs undergoing EVLP in the ACA group, EVLP was terminated prematurely because of severe lung edema and inability to perfuse the lungs. There were no significant differences in changes of lung oxygenation or pulmonary vascular resistance between groups. Compliance decreased and lung weights increased in both groups, but more in the ACA group (p = 0.083 and p = 0.065, respectively). There was no obvious difference in gene expression for hypoxia inducible factor-1α, inflammatory markers, free radicals, or lung injury between groups. CONCLUSIONS: Lung edema formation and decreased lung compliance occurs with both EVLP techniques but were more pronounced in the ACA group. Otherwise, there were no differences in lung function, inflammatory response, ischemia/reperfusion injury, or histopathologic changes between the EVLP techniques.
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OBJECTIVES: Ischaemia-reperfusion injury is a necessary part of organ transplantation and a key determinant of both acute and chronic graft failure. We have assessed the contribution of endothelial nitric oxide synthase (eNOS) and eNOS uncoupling to oxidative and nitrosative stress formation during lung ischaemia-reperfusion injury dependent on ischaemia time. METHODS: Forty eNOS wild-type mice (eNOS +/+ ) and 40 eNOS knock-out mice (eNOS -/- ) received either a sham thoracotomy or 60 or 90 min of ischaemia, followed by 0, 1 or 24 h of reperfusion. Lung tissue was analysed with electron spin resonance for NO production and reactive oxygen species content. Protein nitrosation, eNOS and eNOS uncoupling were determined using western blotting. In peripheral blood, arterial blood gases were taken and reactive oxygen species content was determined. RESULTS: eNOS +/+ mice had lower reactive oxygen species production in their peripheral circulation but worse blood gas values after 1 h of reperfusion. Lung tissue of eNOS -/- mice showed lower reactive oxygen species and NO production and lower protein nitrosation compared with wild-type mice. Longer ischaemia times result in more elaborate oxidative and nitrosative stress dependent on eNOS genotype. Structural eNOS uncoupling was present after 60 min of ischaemia but diminished after 90 min of ischaemia. CONCLUSIONS: eNOS uncoupling may contribute to lung ischaemia-reperfusion injury and inflammation. This ultimately leads to worse clinical outcome. Stabilizing eNOS may therefore be a new approach to extend pulmonary graft survival.
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Pulmón/metabolismo , Óxido Nítrico Sintasa de Tipo III/metabolismo , Estrés Oxidativo/fisiología , Daño por Reperfusión/metabolismo , Animales , Dióxido de Carbono/sangre , Espectroscopía de Resonancia por Spin del Electrón , Femenino , Concentración de Iones de Hidrógeno , Pulmón/fisiopatología , Ratones , Ratones Noqueados , Óxido Nítrico Sintasa de Tipo III/genética , Estrés Nitrosativo/fisiología , Oxígeno/sangre , Daño por Reperfusión/fisiopatologíaRESUMEN
Dipeptidyl peptidase 4 (DPP4) is a cell surface protease that has been reported to play a role in glucose homeostasis, cancer, HIV, autoimmunity, immunology and inflammation. A role for DPP4 in ischemia-reperfusion injury (IRI) in the heart has been established. Dipeptidyl peptidase 4 inhibition (DPP4i) appeared to decrease infarct size, improves cardiac function and promotes myocardial regeneration. Lung ischemia reperfusion injury is caused by a complex mechanism in which macrophages and neutrophils play an important role. Generation of reactive oxygen species (ROS), uncoupling of nitric oxide synthase (NOS), activation of nuclear factor-κB (NF-κB), activation of nicotinamide adenine dinucleotide phosphate metabolism, and generation of pro-inflammatory cytokines lead to acute lung injury (ALI). In this review we present the current knowledge on DPP4 as a target to treat IRI in the lung. We also provide evidence of the roles of the DPP4 substrates glucagon-like peptide 1 (GLP-1), vasoactive intestinal peptide (VIP) and stromal cell-derived factor-1α (SDF-1α) in protection against oxidative stress through activation of the mitogen-activated protein kinase (MAPK) 1/2 and phosphatidylinositol 3'-kinase (PI3K)/Akt signal transduction pathways.
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Oxidative and nitrosative stress are an umbrella term for pathophysiological processes that involve free radical generation during inflammation. In this review, the involvement of reactive oxygen and nitrogen species is evaluated during lung ischemia-reperfusion injury (LIRI) from a surgical point of view. The main biochemical and cellular mechanisms behind free radical generation are discussed, together with surgical procedures that may cause reperfusion injury. Finally, different therapeutic strategies are further explored. A literature search was performed, searching for "lung ischemia reperfusion injury", "reperfusion injury", "large animal model" and different search terms for each section: "surgery", "treatment", "cellular mechanism", or "enzyme". Although reperfusion injury is not an uncommon entity and there is a lot of evidence concerning myocardial ischemia-reperfusion injury, in the lung this phenomenon is less extensively described and studies in large animals are not easy to come by. With increasing number of patients on waiting lists for lung transplant, awareness for this entity should all but rise.
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It was recently proposed that bactericidal antibiotics, besides through specific drug-target interactions, kill bacteria by a common mechanism involving the production of reactive oxygen species (ROS). However, this mechanism involving the production of hydroxyl radicals has become the subject of a lot of debate. Since the contribution of ROS to antibiotic mediated killing most likely depends on the conditions, differences in experimental procedures are expected to be at the basis of the conflicting results. In the present study different methods (ROS specific stainings, gene-expression analyses, electron paramagnetic resonance, genetic and phenotypic experiments, detection of protein carbonylation and DNA oxidation) to measure the production of ROS upon antibiotic treatment in Burkholderia cepacia complex (Bcc) bacteria were compared. Different classes of antibiotics (tobramycin, ciprofloxacin, meropenem) were included, and both planktonic and biofilm cultures were studied. Our results indicate that some of the methods investigated were not sensitive enough to measure antibiotic induced production of ROS, including the spectrophotometric detection of protein carbonylation. Secondly, other methods were found to be useful only in specific conditions. For example, an increase in the expression of OxyR was measured in Burkholderia cenocepacia K56-2 after treatment with ciprofloxacin or meropenem (both in biofilms and planktonic cultures) but not after treatment with tobramycin. In addition results vary with the experimental conditions and the species tested. Nevertheless our data strongly suggest that ROS contribute to antibiotic mediated killing in Bcc species and that enhancing ROS production or interfering with the protection against ROS may form a novel strategy to improve antibiotic treatment.
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Antibacterianos/farmacocinética , Infecciones por Burkholderia/metabolismo , Complejo Burkholderia cepacia/metabolismo , Especies Reactivas de Oxígeno/metabolismo , Antibacterianos/farmacología , Biopelículas/efectos de los fármacos , Biopelículas/crecimiento & desarrollo , Infecciones por Burkholderia/tratamiento farmacológico , Infecciones por Burkholderia/microbiología , Complejo Burkholderia cepacia/efectos de los fármacos , Complejo Burkholderia cepacia/crecimiento & desarrollo , Muerte Celular/efectos de los fármacos , Ciprofloxacina/farmacología , Regulación Bacteriana de la Expresión Génica/efectos de los fármacos , Meropenem , Pruebas de Sensibilidad Microbiana , Proteínas Represoras/biosíntesis , Tienamicinas/farmacología , Tobramicina/farmacologíaRESUMEN
OBJECTIVES: Pulmonary ischaemia-reperfusion injury (IRI) is associated with several life-threatening pulmonary disorders, and may severely compromise the outcome of lung transplantation. Highly reactive molecules such as superoxide, nitric oxide (NO) and peroxynitrite (ONOO(-)) are presumed to contribute to IRI pathogenesis, but this assumption is based on indirect measurements. We use electron spin resonance (ESR) to directly quantify free radical formation after pulmonary ischaemia and reperfusion. METHODS: Five groups of 10 Swiss mice were subjected to left pulmonary hilum clamping for 1 h of ischaemia followed by 0, 1, 4 and 24 h of reperfusion or to sham thoracotomy alone as control procedure. In five mice per group, ESR was used to measure iron-diethyldithio-carbamate trihydrate-trapped NO in the lung. In the other group of 5, reactive oxygen species generation in the lung and in blood was quantified with ESR by detection of ascorbyl radical and CMH spin probe, respectively. Pulmonary ONOO(-) was monitored with nitrotyrosine Western blotting. RESULTS: After 1 h of reperfusion, a pulmonary NO peak (14.69 ± 0.91 × 10(4) Arbitrary Units (A.U.). vs 1.84 ± 0.75 × 10(4) A.U. in sham; P < 0.001) coincided with a significant increase in nitrosated proteins (0.105 ± 0.015 A.U.) compared with sham (0.047 ± 0.006 A.U.); P < 0.005). Peripheral blood showed a significant free radical burst after 1 h of ischaemia (11 774 ± 728 A.U. vs 6660 ± 833 A.U. in sham; P < 0.001). CONCLUSIONS: Longitudinal quantification of free radicals during IRI reveals the occurrence of two major radical bursts. The radical peak in peripheral blood after ischaemia may be related to systemic hypoxia. After 1 h of reperfusion, the lung tissue shows a significant increase of superoxide, NO and their reaction products, which are probably involved in IRI pathogenesis.
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Radicales Libres/metabolismo , Pulmón/irrigación sanguínea , Daño por Reperfusión/metabolismo , Daño por Reperfusión/fisiopatología , Animales , Modelos Animales de Enfermedad , Espectroscopía de Resonancia por Spin del Electrón/métodos , Estudios de Evaluación como Asunto , Femenino , Trasplante de Pulmón/efectos adversos , Ratones , Óxido Nítrico/metabolismo , Estrés Oxidativo/fisiología , Distribución Aleatoria , Especies Reactivas de Oxígeno/metabolismo , Sensibilidad y Especificidad , Superóxido Dismutasa/metabolismoRESUMEN
Pulmonary ossifications are classified as either dendriform or nodular, according to their histologic appearance. Both seem to be distributed similarly and are often confined to the lower lobes of the lung. These ossifications may be included in the differential diagnosis of a solitary pulmonary nodule.
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Adenocarcinoma/patología , Enfermedades Pulmonares/patología , Neoplasias Pulmonares/patología , Osificación Heterotópica/patología , Nódulo Pulmonar Solitario/patología , Adenocarcinoma/diagnóstico , Adenocarcinoma/cirugía , Anciano , Diagnóstico Diferencial , Humanos , Pulmón/patología , Pulmón/cirugía , Enfermedades Pulmonares/diagnóstico , Enfermedades Pulmonares/cirugía , Neoplasias Pulmonares/diagnóstico , Neoplasias Pulmonares/cirugía , Masculino , Osificación Heterotópica/diagnóstico , Osificación Heterotópica/cirugía , Tomografía de Emisión de Positrones , Nódulo Pulmonar Solitario/diagnóstico , Nódulo Pulmonar Solitario/cirugía , Toracotomía , Tomografía Computarizada por Rayos XRESUMEN
The homodimeric flavohemeprotein endothelial nitric oxide synthase (eNOS) oxidizes l-arginine to l-citrulline and nitric oxide (NO), which acutely vasodilates blood vessels and inhibits platelet aggregation. Chronically, eNOS has a major role in the regulation of blood pressure and prevention of atherosclerosis by decreasing leukocyte adhesion and smooth muscle proliferation. However, a disturbed vascular redox balance results in eNOS damage and uncoupling of oxygen activation from l-arginine conversion. Uncoupled eNOS monomerizes and generates reactive oxygen species (ROS) rather than NO. Indeed, eNOS uncoupling has been suggested as one of the main pathomechanisms in a broad range of cardiovascular and pulmonary disorders such as atherosclerosis, ventricular remodeling, and pulmonary hypertension. Therefore, modulating uncoupled eNOS, in particular eNOS-dependent ROS generation, is an attractive therapeutic approach to preventing and/or treating cardiopulmonary disorders, including protective effects during cardiothoracic surgery. This review provides a comprehensive overview of the pathogenetic role of uncoupled eNOS in both cardiovascular and pulmonary disorders. In addition, the related therapeutic possibilities such as supplementation with the eNOS substrate l-arginine, volatile NO, and direct NO donors as well as eNOS modulators such as the eNOS cofactor tetrahydrobiopterin and folic acid are discussed in detail.