Navegando por Palavras-chave "ARDS"

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    Acute lung injury is reduced by the alpha 7nAChR agonist PNU-282987 through changes in the macrophage profile
    (Federation Amer Soc Exp Biol, 2017) Pinheiro, Nathalia Montouro; Santana, Fernanda Paula Roncon [UNIFESP]; Almeida, Rafael Ribeiro; Guerreiro, Marina [UNIFESP]; Martins, Milton de Arruda; Caperuto, Luciana Chagas [UNIFESP]; Câmara, Niels Olsen Saraiva; Wensing, Lislaine Andrade; Prado, Vânia Ferreira; Tibério, Iolanda de Fátima Lopes Calvo; Prado, Marco Antônio Máximo; Prado, Carla Maximo [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Nicotinic alpha-7 acetylcholine receptor (nAChR alpha 7) is a critical regulator of cholinergic anti-inflammatory actions in several diseases, including acute respiratory distress syndrome (ARDS). Given the potential importance of alpha 7nAChR as a therapeutic target, we evaluated whether PNU-282987, an alpha 7nAChR agonist, is effective in protecting the lung against inflammation. We performed intratracheal instillation of LPS to generate acute lung injury (ALI) in C57BL/6mice. PNU-282987 treatment, either before or after ALI induction, reduced neutrophil recruitment and IL1 beta, TNF-alpha, IL-6, keratinocyte chemoattractant (KC), and IL-10 cytokine levels in the bronchoalveolar lavage fluid (P<0.05). In addition, lung NF-kappa B phosphorylation decreased, along with collagen fiber deposition and the number of matrix metalloproteinase-9(+) and -2(+) cells, whereas the number of tissue inhibitor of metalloproteinase-1(+) cells increased (P < 0.05). PNU-282987 treatment also reduced lung mRNA levels and the frequency of M1 macrophages, whereas cells expressing the M2-related markers CD206 and IL-10 increased, suggesting changes in the macrophage profile. Finally, PNU-282987 improved lung function in LPS-treated animals. The collective results suggest that PNU-282987, anagonist of alpha 7nAChR, reduces LPS-induced experimental ALI, thus supporting the notion that drugs that act on alpha 7nAChRs should be explored for ARDS treatment in humans.-Pinheiro, N. M., Santana, F. P. R., Almeida, R. R., Guerreiro, M., Martins, M. A., Caperuto, L. C., Camara, N. O. S., Wensing, L. A., Prado, V. F., Tiberio, I. F. L. C., Prado, M. A. M., Prado, C. M. Acute lung injury is reduced by the alpha 7nAChR agonist PNU-282987 through changes in the macrophage profile.
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    Efeito da posição prona sem PEEP na oxigenação e complacência em modelo experimental com lesão pulmonar
    (Sociedade Brasileira de Pediatria, 2007-08-01) Yagui, Ana Cristina Zanon [UNIFESP]; Beppu, Osvaldo Shigueomi [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    OBJECTIVE: To observe the effects of the prone position and the need for positive end-expiratory pressure (PEEP) to improve oxygenation. METHODS: Sixteen rats were anesthetized and ventilated at a tidal volume of 8 mL/kg, respiratory rate of 60 rpm and PEEP = 0 cmH2O (ZEEP), in the supine position for 30 minutes. Lung injury was then induced by means of intratracheal instillation of hydrochloric acid. Once the injury was established, rats were placed in the prone position for a further 30 minutes and randomized into two groups: in group 1 PEEP = 5 cmH2O was added; while group 2 was kept on ZEEP. Measurements of pulmonary mechanics, arterial blood gas analysis and mean arterial pressure were taken at the end of each phase. RESULTS: In group 1, oxygen partial pressure increased significantly from 98.7±26.5 to 173.9±58.4 mmHg between injury and prone phases; in group 2 it was unchanged, varying from 99.6±15.4 to 100.5±24.5 mmHg. Group 1 also exhibited significant improvement in complacency, from 0.20±0.01 to 0.23±0.02 mL/cmH2O, while, once more, group 2 did not exhibit improvement, going from 0.21±0.02 to 0.22±0.01 mL/cmH2O. Mean arterial blood pressure measurements did not change significantly in either group at any point during the experiment. CONCLUSIONS: The prone position only resulted in improved oxygenation and respiratory mechanics when combined with PEEP = 5 cmH2O. The prone position did not cause hemodynamic compromise with or without PEEP = 5 cmH2O.
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    Mechanical Ventilation in Sepsis: A Reappraisal
    (Lippincott Williams & Wilkins, 2017) Zampieri, Fernando G.; Mazza, Bruno Franco [UNIFESP]
    Sepsis is the main cause of close to 70% of all cases of acute respiratory distress syndromes (ARDS). In addition, sepsis increases susceptibility to ventilator-induced lung injury. Therefore, the development of a ventilatory strategy that can achieve adequate oxygenation without injuring the lungs is highly sought after for patients with acute infection and represents an important therapeutic window to improve patient care. Suboptimal ventilatory settings cannot only harm the lung, but may also contribute to the cascade of organ failure in sepsis due to organ crosstalk. Despite the prominent role of sepsis as a cause for lung injury, most of the studies that addressed mechanical ventilation strategies in ARDS did not specifically assess sepsis-related ARDS patients. Consequently, most of the recommendations regarding mechanical ventilation in sepsis patients are derived from ARDS trials that included multiple clinical diagnoses. While there have been important improvements in general ventilatory management that should apply to all critically ill patients, sepsis-related lung injury might still have particularities that could influence bedside management. After revisiting the interplay between sepsis and ventilation-induced lung injury, this review will reappraise the evidence for the major components of the lung protective ventilation strategy, emphasizing the particularities of sepsis-related acute lung injury.