Positive pressure ventilation (PPV) is one of the most commonly used treatment modalities in the field of neonatology to achieve adequate gas exchange for infants with respiratory difficulties. However, mechanical ventilation may cause lung injury through various mechanisms, including high airway pressure and high tidal volume, leading to acute respiratory distress syndrome, bronchopulmonary dysplasia or multiple organ failure. To prevent these injuries, clinicians, especially neonatologists, treating premature infants with respiratory distress syndrome, should be familiar with ventilator-induced lung injury and its preventive strategies. In this review, the mechanisms of lung injury, the effects of mechanical ventilation on pulmonary microvascular endothelium, extracelluar matrix and alveolar epithelium, and lung protective strategies of conventional ventilation are introduced. Several forms of conventional ventilation for preterm infants are also described.
Acute Lung Injury ; Bronchopulmonary Dysplasia ; Endothelium ; Epithelium ; Humans ; Infant ; Infant, Newborn ; Infant, Premature ; Lung ; Lung Injury ; Multiple Organ Failure ; Neonatology ; Positive-Pressure Respiration ; Respiration, Artificial ; Respiratory Distress Syndrome, Adult ; Tidal Volume ; Ventilation ; Ventilator-Induced Lung Injury

No abstract available.
Acute Lung Injury* ; Lung*

A High concentration of oxygen (>40%) is used as a life-saving therapy in preterm newborns since birth. By generating excess reactive oxygen species, however, hyperoxia can cause lung injury leading to bronchopulmonary dysplasia (BPD). Although hyperoxia-induced lung injury contributes to the evolution of BPD, the mechanisms by which hyperoxia contributes to the genesis of lung injury in preterm lungs are not yet fully defined, and there are no specific measures for the protection of preterm lungs against injury secondary to hyperoxia. Alveolar type II cells are key components of the alveolar structure, and they are responsible for the restoration of normal alveolar epithelium after acute lung injury. However, hyperoxia is primarily delivered to the alveolar epithelium and alveolar type II cells can be the main target for the injury secondary to hyperoxia. To date, my researches have been focused on injury of fetal alveolar type II cells exposed to hyperoxia and the role of anti-inflammatory cytokine, IL-10 minimizing fetal type II cell injury induced by hyperoxia. Based on my previous studies, this article summarizes the cellular and molecular mechanisms of fetal type II cell injury induced in the early stage of hyperoxia and the protective potency of IL-10 in fetal alveolar type II cells and neonatal lungs injured by hyperoxia.
Acute Lung Injury ; Bronchopulmonary Dysplasia ; Epithelium ; Humans ; Hyperoxia ; Infant, Newborn ; Interleukin-10 ; Lung ; Lung Injury ; Oxygen ; Parturition ; Reactive Oxygen Species

No abstract available.
Acute Lung Injury*

No abstract available.
Acute Lung Injury* ; Cytokines*

No abstract available.
Acute Lung Injury*

No abstract available.
Acute Lung Injury* ; Genomics*

BACKGROUND: Since the late 1960s, mechanical ventilation has been accomplished primarily using volume controlled ventilation(VCV). While VCV allows a set tidal volume to be guaranteed, VCV could bring about excessive airway pressures that may be lead to barotrauma in the patients with acute lung injury. With the increment of knowledge related to ventilator-induced lung injury, pressure controlled ventilation(PCV) has been frequenfly applied to these patients. But, PCV has a disadvantage of variable tidal volume delivery as pulinonary impedance changes. Since the concept of combining the positive attributes of VCV and PCV(dual control ventilation, DCV) was described firstly in 1992, a few DCV modes were introduced. Pressure-regulated volume control(PRVC) mode, a kind of DCV, is pressure-limited, time-cycled ventilation that uses tidal volume as a feedback control for continuously adjusting the pressure limit. However, no clinical studies were published on the efficacy of PRVC until now. This investigation studied the efficacy of PRVC in the patients with unstable respiratory mechanics. METHODS: The subjects were 8 mechanically ventilated patients(M: F= 6 : 2, 56+/-26 years) who showed unstable respiratory mechanics, which was defined by the coefficients of variation of peak inspiratory pressure for 15 minutes greater than 10% under VCV, or the coefficients of variation of tidal volume greater than 10% under PCV. The study was consisited of 3 modes application with VCV, PCV and PRVC for 15 minutes by random order. To obtain same tidal volume, inspiratory pressure setting was adjusted in PCV. Respiratory parameters were measured by pulmonary monitor(CP-100 pulmonary monitor, Bicore, Irvine, CA, USA). RESULTS: 1) Mean tidal volumes(VT) in each mode were not different(VCV, 431+/-102ml ; PCV, 417+/-99ml; PRVC, 414+/-97ml) 2) The coefficient of variation(CV) of VT were 5.2+/-3.9% in VCV, 15.2+/-7.5% in PCV and 19.3+/-10.0% in PRVC. The CV of VT in PCV and PRVC were significantly greater than that in VCV(p<0.01). 3) Mean peak inspiratory pressure(PIP) in VCV(31.0+/-6.9cm HD) was higher than PIP in PCV(26.0+/-6.5cm H20) or PRVC(27.0+/-6.4cm HD)(p<0.05). 4) The CV of PIP were 13.9+/-3.7% in VCV, 4.9+/-2.6% in PVC and 12.2+/-7.0% in PRVC. The CV of PIP in VCV and PRVC were greater than that in PCV(p<0.01). CONCLUSIONS: Because of wide fluctuations of VT and PIP, PRVC mode did not seem to have advantages compared to VCV or PCV in the patients with unstable respiratory mechanics.
Acute Lung Injury ; Barotrauma ; Electric Impedance ; Humans ; Respiration, Artificial ; Respiratory Mechanics* ; Tidal Volume ; Ventilation ; Ventilator-Induced Lung Injury

BACKGROUND: Experimentally, maintaining high pressure or high volume ventilation in animal models produces an acute lung injury, however, there was little information on remodeling. We investigated the collagen synthesis in a rat model of ventilator-induced lung injury. METHODS: Rats were ventilated with room air at 85 breaths/minute for 2 hours either tidal volume 7 ml/kg or 20 ml/kg (V(T)7 or V(T)20, respectively). After 2 hours of ventilation, rats were placed in the chamber for 24 hours. Lung collagen was evaluated by immunohistochemistry (n=5) and collagen was quantitated by collagen assay (n=5). Static compliance (Csta) of the whole lung as obtained from the pressure volume curves. RESULTS: Type I collagen was an increase in expression in the interstitium with large V(T) (20 ml/ kg) ventilation after 2 hours of mechanical ventilation (MV), and further increased expression after 24 hours of recovery period. Static lung compliance was significantly (p<0.05) decreased in the V(T)20 compared with V(T)7 (0.221+/-0.05 vs 0.305+/-0.06 ml/cm H2O) after 2 hours of MV. There was a further decrease in lung compliance after 24 hours of recovery period (0.144+/-0.07 vs 0.221+/-0.05, p<0.05) in the V(T)20. CONCLUSIONS: Large tidal volume ventilation causes an increase in type 1 collagen expression with reduction of lung compliance.
Acute Lung Injury ; Animals ; Collagen Type I ; Collagen* ; Compliance ; Immunohistochemistry ; Lung ; Lung Compliance ; Models, Animal* ; Rats* ; Respiration, Artificial ; Tidal Volume ; Ventilation ; Ventilator-Induced Lung Injury*

BACKGROUND: Adaptive support ventilation (ASV), an automated closed-loop ventilation mode, adapts to the mechanical characteristics of the respiratory system by continuous measurement and adjustment of the respiratory parameters. The adequacy of ASV was evaluated in the patients with acute lung injury (ALI). METHODS: A total of 36 patients (19 normal lungs and 17 ALIs) were enrolled. The patients' breathing patterns and respiratory mechanics parameters were recorded under the passive ventilation using the ASV mode. RESULTS: The ALI patients showed lower tidal volumes and higher respiratory rates (RR) compared to patients with normal lungs (7.1+/-0.9 mL/kg vs. 8.6+/-1.3 mL/kg IBW; 19.7+/-4.8 b/min vs. 14.6+/-4.6 b/min; p<0.05, respectively). The expiratory time constant (RCe) was lower in ALI patients than in those with normal lungs, and the expiratory time/RCe was maintained above 3 in both groups. In all patients, RR was correlated with RCe and peak inspiratory flow (rs=-0.40; rs=0.43; p<0.05, respectively). In ALI patients, significant correlations were found between RR and RCe (rs=-0.76, p<0.01), peak inspiratory flow and RR (rs=-0.53, p<0.05), and RCe and peak inspiratory flow (rs=-0.53, p<0.05). CONCLUSION: ASV was found to operate adequately according to the respiratory mechanical characteristics in the ALI patients. Discrepancies with the ARDS Network recommendations, such as a somewhat higher tidal volume, have yet to be addressed in further studies.
Acute Lung Injury ; Automation ; Humans ; Lung ; Respiration ; Respiratory Mechanics ; Respiratory Rate ; Respiratory System ; Tidal Volume ; Ventilation ; Ventilator-Induced Lung Injury ; Ventilators, Mechanical