Nitrogen dioxide and other nitrous oxides are rapidly generated when nitric acid comes in contact with air or organic materials. After inhalation, structural lung injury becomes manifest mainly in the distal bronchioles and adjacent alveoli. This localization may reflect greater cellular solubilization of NO* at these levels than at more proximal levels and/or the airflow dynamics. The subsequent cellular damage is attributed to the formation of chemical-free radicals and of nitric and nitrous acids from hydration of NOa. These time-dependent interactions account, in part, for the delayed manifestations of lung injury. The pulmonary edema correlates with necrosis of alveolar epithelium and/or endothelium.
Our light microscopy findings generally are similar to those previously reported. However, electron microscopy revealed alveolar capillaries containing many degranulated and necrotic neutrophils together with necrotic endothelial cells. Sequestration of activated neutrophils within lung capillaries has been observed in acute lung injury resulting from various direct and indirect insults that result in increased microvascular permeability and edema. The release of neutrophil enzymes and free radicals and the activation of mediators from leaked plasma often have been incriminated in the progression of microvascular injury, thus amplifying or sustaining the injury, which was initiated in our patients by NOa. The demargination granulocytosis and hemoconcentration, observed in experimental NOa exposures and here (Table 1), may be relevant to that mechanism. Viagra Professional
The edema fluid contained serum albumin, IgG, IgM and fibrinogen, indicating markedly increased capillary permeability. IgM and fibrinogen were relatively restricted to alveolar ducts, where both interstitial and hyaline membrane staining were evident. In contrast, IgG and albumin were more evenly distributed in the edema fluid with little detected in the interstitium, suggesting a more ready diffusion of these smaller molecules. It is unknown whether altered immunoglobulins in the interstitium were stimuli for the neutrophil accumulation and/or activation in alveolar capillaries.