Tables
- TABLE 1
Time of onset of pathological findings of pulmonary oxygen toxicity (POT) in primates and humans
Day POT phase Primates Day POT phase Humans 1 1 Tracheobroncholitis, mucous flow decreased 2 Exudation Alveolar oedema, septal wall oedema, distention lymphatic vessels, decrement alveolar type 1 cells 2–5 Exudation Denuded alveolar type 1 cells, oedematous endothelial capillary cell swelling, necrosis respiratory epithelium, squamous metaplasia tracheal and bronchial mucosa, deposition eosinophilic slough, alveolar and interstitial oedema, formation hyaline membrane, cilial loss, decreased mucociliary transport 4 Resolution, formation hyaline membrane, influx inflammatory cells 5 Proliferation Increment alveolar type 2 cells, fibroblast infiltration 5–88 Proliferation Proliferation of alveolar type 2 replacing alveolar type 1 cells, derangement of collagen and elastin, incorporation of hyaline membranes into the septal walls, fibroblastic proliferation, collagen fibre deposition, fibro-proliferative organisation of intra-alveolar exudate, infiltration with inflammatory cells, interstitial lung fibrosis, emphysematous alveoli with areas of fibrosis, cilial loss 8 Intra-alveolar hyaline membranes, thickening of the alveolar-capillary membrane, leukocytic infiltration, marked cellular proliferation of abnormal alveolar type 2 cells, haemorrhagic areas, accumulation of intracellular water 12 Extravascular lung water within the pulmonary parenchyma and interstitial space, invasion of fibroblasts and macrophages 56 Air-blood barrier thickened, increase in collagen content, intra-alveolar septal scarring, alveolar air volume diminished - TABLE 2
Corresponding median decrease in vital capacity (VC) based on total units of pulmonary dose (UPTD)
UPTD % median decrease in VC 615 2 825 4 1035 6 1230 8 1425 10 1815 15 2190 20 Data from [48].
- TABLE 3
Pathological findings in pulmonary oxygen toxicity and their changes in lung function parameters
Pathological changes Increase in parameter Decrease in parameter Interstitial oedema VC, DLCO, CL,st Alveolar oedema VC, DLCO, CL,st Pulmonary capillary fibrin thrombin VC, DLCO, FeNO Loss of alveolar type 1 cell VC, DLCO, CL,st Neutrophilic infiltration FeNO FeNO Capillary endothelial lesions VC, DLCO, CL,st Interstitial distention DLCO Increase alveolar type 2 cells CL,st DLCO Infiltration inflammatory cells FeNO Haemorrhage DLCO VC: vital capacity; DLCO: diffusing capacity of the lung for carbon monoxide; CL,st: static lung compliance; FeNO: exhaled nitric oxide fraction. Data from [58].
Vol 25 Issue 142
Table of Contents
Oxygen, the lung and the diver: friends and foes?
