Browsing by Author "Salomon, Tatiana"
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Item Mild hypothermia increases pulmonary anti-inflammatory response during protective mechanical ventilation in a piglet model of acute lung injury(John Wiley & Sons, 2013) Cruces, Pablo; Erranz, Benjamín; Donoso, Donoso; Carvajal, Cristobal; Salomon, Tatiana; Torres, Maria; Diaz, FrancoBACKGROUND: The effects of mild hypothermia (HT) on acute lung injury (ALI) are unknown in species with metabolic rate similar to that of humans, receiving protective mechanical ventilation (MV). We hypothesized that mild hypothermia would attenuate pulmonary and systemic inflammatory responses in piglets with ALI managed with a protective MV. METHODS: Acute lung injury (ALI) was induced with surfactant deactivation in 38 piglets. The animals were then ventilated with low tidal volume, moderate positive end-expiratory pressure (PEEP), and permissive hypercapnia throughout the experiment. Subjects were randomized to HT (33.5°C) or normothermia (37°C) groups over 4 h. Plasma and tissue cytokines, tissue apoptosis, lung mechanics, pulmonary vascular permeability, hemodynamic, and coagulation were evaluated. RESULTS: Lung interleukin-10 concentrations were higher in subjects that underwent HT after ALI induction than in those that maintained normothermia. No difference was found in other systemic and tissue cytokines. HT did not induce lung or kidney tissue apoptosis or influence lung mechanics or markers of pulmonary vascular permeability. Heart rate, cardiac output, oxygen uptake, and delivery were significantly lower in subjects that underwent HT, but no difference in arterial lactate, central venous oxygen saturation, and coagulation test was observed. CONCLUSIONS: Mild hypothermia induced a local anti-inflammatory response in the lungs, without affecting lung function or coagulation, in this piglet model of ALI. The HT group had lower cardiac output without signs of global dysoxia, suggesting an adaptation to the decrease in oxygen uptake and delivery. Studies are needed to determine the therapeutic role of HT in ALI.Item Near-apneic ventilation decreases lung injury and fibroproliferation in an ARDS model with ECMO(2019) Araos, Joaquín; Alegría, Leyla; Garcia, Patricio; Cruces, Pablo; Soto, Dagoberto; Erranz, Benjamín; Amthauer, Macarena; Salomon, Tatiana; Medina, Tania; Rodríguez, Felipe; Ayala, Pedro; Borzone, Gisella R.; Meneses, Manuel; Damiani, Felipe; Retamal, Jaime; Cornejo, Rodrigo; Bugedo, Guillermo; Bruhn, AlejandroRationale: There is wide variability in mechanical ventilation settings during ECMO in ARDS patients. Although lung rest is recommended to prevent further injury, there is no evidence to support it. Objectives: To determine whether near-apneic ventilation decreases lung injury in a pig model of ARDS supported with ECMO. Methods: Pigs (26-36kg; n=24) were anesthetized and connected to mechanical ventilation. In 18 animals lung injury was induced by a double-hit consisting in repeated saline lavages followed by 2 hours of injurious ventilation. Then, animals were connected to high-flow veno-venous ECMO, and randomized into 3 groups: Non-protective (PEEP 5 cmH2O, tidal volume 10 ml/kg, respiratory rate 20 bpm); Conventional-protective (PEEP 10 cmH2O, tidal volume 6 ml/kg, respiratory rate 20 bpm); Near-apneic (PEEP 10 cmH2O, driving pressure 10 cmH2O, respiratory rate 5 bpm). Six other pigs were used as Sham. All groups were maintained during the 24-hour study period. Measurements and Main Results: Minute ventilation and mechanical power were lower in the Near-apneic group, but no differences were observed in oxygenation or compliance. Lung histology revealed less injury in the Near-apneic group. Extensive immunohistochemical staining for myofibroblasts and pro-collagen III was observed in the Non-protective group, with the Near-apneic group exhibiting the least alterations. Near- apneic group showed significantly less matrix-metalloproteinase-2 and -9 activity. Histological lung injury and fibroproliferation scores were positively correlated with driving pressure and mechanical power.Item Surfactant deactivation in a pediatric model induces hypovolemia and fluid shift to the extravascular lung compartment(John Wiley & Sons, 2013) Diaz, Franco; Erranz, Benjamín; Donoso, Alejandro; Carvajal, Cristobal; Salomon, Tatiana; Torres, Maria; Cruces, PabloBACKGROUND: Surfactant deficiency is the pivotal abnormality in Neonatal and Acute Respiratory Distress Syndrome. Surfactant deactivation can produce hypoxemia, loss of lung compliance, and pulmonary edema, but its circulatory consequences are less understood. OBJECTIVE: To describe the sequential hemodynamic changes and pulmonary edema formation after surfactant deactivation in piglets. METHODS: Surfactant deactivation was induced by tracheal instillation of polysorbate 20 in 15 anesthetized and mechanically ventilated Large White piglets. The hemodynamic consequences of surfactant deactivation were assessed at 30, 120, and 240 min by transpulmonary thermodilution and traditional methods. RESULTS: Surfactant deactivation caused hypoxemia, reduced lung compliance, and progressively increased lung water content (P < 0.01). Early hypovolemia was observed, with reductions of the global end-diastolic volume and stroke volume (P < 0.05). Reduced cardiac output was observed at the end of the study (P < 0.05). Standard monitoring was unable to detect these early preload alterations. Surprisingly, the bronchoalveolar protein content was greatly increased at the end of the study compared with baseline levels (P < 0.01). This finding was inconsistent with the notion that the pulmonary edema induced by surfactant deactivation was exclusively caused by high surface tension. CONCLUSIONS: Hypovolemia develops early after surfactant deactivation, in part due to the resulting fluid shift from the intravascular compartment to the lungs.