Pulmonary edema

About: Pulmonary edema is a research topic. Over the lifetime, 8721 publications have been published within this topic receiving 222094 citations. The topic is also known as: pulmonary oedema & edema pulmonary.

Angiotensin-converting enzyme 2 protects from severe acute lung failure

Abstract: Acute respiratory distress syndrome (ARDS), the most severe form of acute lung injury, is a devastating clinical syndrome with a high mortality rate (30-60%) (refs 1-3). Predisposing factors for ARDS are diverse and include sepsis, aspiration, pneumonias and infections with the severe acute respiratory syndrome (SARS) coronavirus. At present, there are no effective drugs for improving the clinical outcome of ARDS. Angiotensin-converting enzyme (ACE) and ACE2 are homologues with different key functions in the renin-angiotensin system. ACE cleaves angiotensin I to generate angiotensin II, whereas ACE2 inactivates angiotensin II and is a negative regulator of the system. ACE2 has also recently been identified as a potential SARS virus receptor and is expressed in lungs. Here we report that ACE2 and the angiotensin II type 2 receptor (AT2) protect mice from severe acute lung injury induced by acid aspiration or sepsis. However, other components of the renin-angiotensin system, including ACE, angiotensin II and the angiotensin II type 1a receptor (AT1a), promote disease pathogenesis, induce lung oedemas and impair lung function. We show that mice deficient for Ace show markedly improved disease, and also that recombinant ACE2 can protect mice from severe acute lung injury. Our data identify a critical function for ACE2 in acute lung injury, pointing to a possible therapy for a syndrome affecting millions of people worldwide every year.

High Inflation Pressure Pulmonary Edema: Respective Effects of High Airway Pressure, High Tidal Volume, and Positive End-expiratory Pressure

Abstract: The respective roles of high pressure and high tidal volume to promote high airway pressure pulmonary edema are unclear. Positive end-expiratory pressure (PEEP) was shown to reduce lung water content in this type of edema, but its possible effects on cellular lesions were not documented. We compared the consequences of normal tidal volume ventilation in mechanically ventilated rats at a high airway pressure (HiP-LoV) with those of high tidal volume ventilation at a high (HiP-HiV) or low (LoP-HiV) airway pressure and the effects of PEEP (10 cm H2O) on both edema and lung ultrastructure. Pulmonary edema was assessed by extravascular lung water content and microvascular permeability by the dry lung weight and the distribution space of 125I-labeled albumin. HiP-LoV rat lungs were not different from those of controls (7 cm H2O peak pressure ventilation). By contrast, the lungs from the groups submitted to high volume ventilation had significant permeability type edema. This edema was more pronounced in LoP-HiV...

The acute respiratory distress syndrome.

Abstract: The acute respiratory distress syndrome (ARDS) is an important cause of acute respiratory failure that is often associated with multiple organ failure. Several clinical disorders can precipitate ARDS, including pneumonia, sepsis, aspiration of gastric contents, and major trauma. Physiologically, ARDS is characterized by increased permeability pulmonary edema, severe arterial hypoxemia, and impaired carbon dioxide excretion. Based on both experimental and clinical studies, progress has been made in understanding the mechanisms responsible for the pathogenesis and the resolution of lung injury, including the contribution of environmental and genetic factors. Improved survival has been achieved with the use of lung-protective ventilation. Future progress will depend on developing novel therapeutics that can facilitate and enhance lung repair.

Experimental pulmonary edema due to intermittent positive pressure ventilation with high inflation pressures. Protection by positive end-expiratory pressure.

Abstract: We used a small animal respirator to ventilate normal, anesthetized rats with room air at peak inspiratory pressures of 14, 30, or 45 cm H2O and no added end-expiratory pressures (intermittent positive pressure breathing [IPPB] 14/0, high inspiratory positive pressure breathing [HIPPB] 30/0, HIPPB 45/0). Other rats were ventilated with the same high inspiratory pressures but with an added end-expiratory pressure of 10 cm H2O (positive end-expiratory pressure [PEEP] 30/10, PEEP 45/10). Control rats that were not ventilated and the IPPB 14/0 group showed no pathologic lung changes. The HIPPB 30/0 and PEEP 30/10 groups had perivascular edema but no alveolar edema. The HIPPB 45/0 animals had alveolar and perivascular edema, severe hypoxemia, and decreased dynamic compliance and died within one hour. In contrast, the PEEP 45/10 animals had no alveolar edema and survived. We postulate that interstitial perivascular edema develops from ventilation with high inflating pressures by mechanisms of lung interdependen...