Publications by authors named "Babu V Naidu"

Background: Operations on structures in the chest (usually the lungs) involve cutting between the ribs (thoracotomy). Severe post-thoracotomy pain can result from pleural (lung lining) and muscular damage, costovertebral joint (ribcage) disruption and intercostal nerve (nerves that run along the ribs) damage during surgery. Poor pain relief after surgery can impede recovery and increase the risks of developing complications such as lung collapse, chest infections and blood clots due to ineffective breathing and clearing of secretions.

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The chest wall, like other regional anatomy, is a remarkable fusion of form and function. Principal functions are the protection of internal viscera and an expandable cylinder facilitating variable gas flow into the lungs. Knowledge of the anatomy of the whole cylinder (ribs, sternum, vertebra, diaphragm, intercostal spaces, and extrathoracic muscles) is therefore not only important in the local environment of a specific chest wall resection but also in its relation to overall function.

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Background: Both tissue sealants and buttressing have been advocated to reduce alveolar air leaks from staple lines following Lung Volume Reduction Surgery (LVRS). However, the long term detrimental effects of buttressing material are increasingly apparent. We performed a pilot prospective randomised self controlled trial in patients undergoing LVRS comparing BioGlue and Peri-strips as adjuncts in preventing alveolar air-leaks.

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Following the acute changes of lung resection surgery, does the ratio of intrathoracic blood volume (ITBV) to global end diastolic volume (GEDV) remain constant? If it does this could validate a single thermo dilution (STD) technique in the measurement of extravascular lung water index (EVLWI) in patients undergoing lung resection surgery. EVLWI was derived using both double dye technique (DDT) and single thermo dilution technique (STD) in four patients undergoing thoracotomy selected for major lung resection surgery. Regular measurements were made for up to 12 h after surgery.

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The management of patients with lung cancer has undergone significant improvement in the last decade in the United Kingdom. The 5-year survival for all patients diagnosed with lung cancer had remained unchanged at 5% over the previous decade, well behind Europe and the United States. Together, government and medical bodies produced guidelines based on best available evidence.

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Background: The activation of poly (adenosine diphosphate) ribose synthetase (PARS) is known to be important in the cellular response to oxidative stress. Previous studies have reported that PARS inhibition confers protection in models of endotoxic shock and ischemia-reperfusion. The purpose of this study was to determine the role of PARS inhibition in lung ischemia-reperfusion injury (LIRI).

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Background: Obliterative bronchiolitis (OB) is the major long-term complication affecting lung transplant recipients, and is characterized pathologically by chronic inflammatory and fibroproliferative airway disease. Based on studies revealing anti-inflammatory and anti-apoptotic properties of poly (ADP)-ribose synthetase (PARS) inhibitors, we hypothesized that their administration would be protective in a heterotopic model of experimental OB.

Methods: We transplanted rat tracheas from Brown-Norway donors into Lewis recipients, and treated 2 groups with a novel PARS inhibitor, INO-1001.

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Background: Alpha chemokines function predominantly to recruit and activate neutrophils, which are important effectors of acute lung injury. This study evaluated whether blockade of 2 potent alpha chemokines, macrophage inflammatory protein-2 (MIP-2) and cytokine-induced neutrophil chemoattractant (CINC), is protective against lung ischemia-reperfusion injury in a warm in situ hilar clamp model.

Methods: Left lungs of Long-Evans rats underwent normothermic ischemia for 90 minutes and reperfusion for up to 4 hours.

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Objective: Tumor necrosis factor-alpha is a proinflammatory mediator required for the development of experimental lung ischemia-reperfusion injury. The alveolar macrophage is a rich source of tumor necrosis factor-alpha in multiple models of acute lung injury. The present study was undertaken to determine whether the alveolar macrophage is an important source of tumor necrosis factor-alpha in lung ischemia-reperfusion injury and whether suppression of its function protects against injury.

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Background: Although chemokines are functionally important in models of ischemia-reperfusion injury, little is known about their role in lung ischemia-reperfusion injury (LIRI). This study examined the role of the beta-chemokines, macrophage inflammatory protein (MIP)-1alpha, monocyte chemoattractant protein (MCP)-1, and regulated upon activation normal T cells expressed and secreted (RANTES) in LIRI.

Methods: Left lungs of Long-Evans rats underwent normothermic ischemia for 90 minutes and reperfusion for up to 4 hours.

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Objectives: We previously demonstrated that calcineurin inhibitors given intravenously ameliorate experimental lung ischemia-reperfusion injury. This study evaluates whether these effects can be achieved when these agents are delivered endotracheally.

Methods: Left lungs of Long Evans rats were rendered ischemic for 90 minutes and reperfused for up to 4 hours.

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Background: Functional roles for chemokines have been demonstrated in several models of ischemia-reperfusion injury. The redundancy inherent to chemokine pathways makes administration of neutralizing antibodies to any single chemokine ineffective in ameliorating injury. This study was undertaken to define the pattern of chemokine expression in lung ischemia-reperfusion injury (LIRI), and to determine whether a broad-spectrum chemokine inhibitor, NR58-3.

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Beta chemokines have been implicated in cardiac and renal allograft rejection. This study determined if antibody antagonization of beta chemokines conferred protection against the development of experimental obliterative bronchiolitis (OB) in a heterotopic rat tracheal allograft model. Rat tracheas were transplanted from Brown-Norway or Lewis donors into Lewis recipients.

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Background: Chemokines are inflammatory mediators that activate and recruit specific leukocyte subpopulations. We have recently shown a role for certain chemokines in a warm in situ rat model of lung ischemia reperfusion injury. After hypoxic stress, rat pulmonary artery endothelial cells (RPAECS) potentiate and direct neutrophil sequestration, and, therefore, contribute to the development of tissue injury.

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Objectives: Statins are lipid-lowering drugs with anti-inflammatory and antioxidant properties. This study explores the potential of these commonly prescribed agents to ameliorate lung ischemia-reperfusion injury.

Methods: Left lungs of Long-Evans rats were rendered ischemic for 90 minutes and reperfused for up to 4 hours.

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Objectives: Activation of the alveolar macrophage is critical to the development of nonischemic inflammatory lung injury. The present studies were undertaken to determine whether the alveolar macrophage plays a similarly important role in lung ischemia-reperfusion injury.

Methods: The left lungs of male rats were rendered ischemic for 90 minutes and reperfused for up to 4 hours.

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Background: Peroxynitrite is a potent cytotoxic free radical produced by the reaction of nitric oxide with the superoxide ion produced in conditions of oxidative stress. The purpose of the study was to examine the role of this reactive nitrogen species in lung ischemia-reperfusion injury.

Methods: Left lungs of male Long-Evans rats were rendered ischemic for 90 minutes and reperfused for up to 4 hours.

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Background: Regulatory cytokines play functional roles in experimental heart, hindlimb, and liver ischemia reperfusion injury. However, little is known about their involvement in direct lung ischemia reperfusion injury (LIRI). These studies were undertaken to investigate the role of two regulatory cytokines, interleukin-4 (IL-4) and IL-10, in an in vivo model of LIRI.

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Obliterative bronchiolitis (OB) affects over half of all survivors following lung or heart-lung transplantation. Respiratory epithelial cell injury, peribronchial inflammation, and proliferation of fibrovascular tissue causing airway occlusion characterize the lesion. While peroxynitrite is known to participate in other models of acute lung injury, its role in the evolution of OB is unclear.

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Background: Obliterative bronchiolitis (OB) affects over half of all long-term survivors after lung transplantation. Respiratory epithelial cell injury, peribronchial inflammation, and proliferation of fibrovascular connective tissue causing airway occlusion characterize this lesion. Several chemokines participate in experimental OB, and singular blockade is only partially effective.

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Objective: Proinflammatory cytokines are known to play roles in ischemia-reperfusion injury of the heart, kidney, small bowel, skin, and liver. Little is known about their roles in ischemia-reperfusion injury of the lung. This study was undertaken to define the role of 2 proinflammatory cytokines, tumor necrosis factor alpha and interleukin 1beta, in ischemia-reperfusion injury of the lung.

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Background: We have recently demonstrated a role for selected chemokines in a rat model of lung ischemia reperfusion injury (LIRI). We have further shown that pretreatment with cyclosporine A (CSA) is protective. The precise cellular events regulating this model are unknown.

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