A common denominator in the etiology of adult respiratory distress syndrome.
The initiating factor in ARDS is a matter of controversy. Some investigators relate ARDS development to diffuse pulmonary microemboli after stress ranging from sepsis to non-thoracic and thoracic trauma. Others indicate hyperoxic exposure as the causative agent. This investigation looked for a common factor in ischemia and hyperoxic exposure in lung which could cause the genesis of ARDS. Studies of oxidative phosphorylation, succinate dehydrogenase activity and ATP level were performed on ischemic and 100% O2 exposed lung. Results in both showed decreased respiration rate below the basal rate, decreased SDH activity, followed by marked decrease in ATP levels in pulmonary tissue. Decrease in respiration (ATP production) capacity and ATP levels in ischemic lung were such that normal cell functions could not be sustained if returned to normal circulation. Hyperbaric O2 therapy would subsequently decrease energy metabolism in regions of normal circulation and in previously ischemic regions.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000328:Adult; D000818:Animals; D004285:Dogs; D006801:Humans; D066298:In Vitro Techniques; D007511:Ischemia / Q000150:complications; D008168:Lung / Q000098:blood supply / Q000378:metabolism; D008928:Mitochondria / Q000378:metabolism; D010085:Oxidative Phosphorylation; D010100:Oxygen; D051381:Rats; D012119:Respiration; D012128:Respiratory Distress Syndrome / Q000209:etiology* / Q000378:metabolism; D013385:Succinate Dehydrogenase / Q000378:metabolism
D000255:Adenosine Triphosphate; D013385:Succinate Dehydrogenase; D010100:Oxygen