Pulmonary hyperbaric oxygen toxicity: preliminary assessment on the role of direct and CNS injury

Abstract

Pulmonary oxygen toxicity has already been extensively studied, but recent studies suggest the influence of concomitant central nervous system (CNS) intoxication, leading to a pulmonary edema, as the cause of pulmonary hyperbaric oxygen toxicity. However, the progressive worsening of pulmonary hyperbaric oxygen toxicity seems to coincide with the development of changes in the pulmonary microcirculation as well as in the distal airways and alveolar-capillary membrane. In view of this, we hypothesized that the local direct toxic effect of oxygen, despite the concomitant intoxication of the CNS, would be decisive for the appearance of pulmonary lesions. Therefore, we propose in this study to evaluate the hyperbaric oxygen effects on rat pulmonary mechanics and structure in different and progressive doses of oxygen, toxic and non-toxic to lung parenchyma in an initial phase. At a later stage we intend to expose the animals to a toxic dose of O2 and effectively evaluate the influence of concomitant intoxication of the CNS through vagal and nitric oxide synthase (NOS) blocade on the variables previously studied in the lung. We hope determine the contribution of direct toxic effect of hyperbaric hyperoxia on ventilatory mechanics and the lung function of gas exchange, thereby assisting in the correct and safe use of oxygen at high concentrations and pressures as occur in medical practice at ICU and hyperbaric oxygen therapy. (AU)