Journal of physiology and pharmacology : an official journal of the Polish Physiological Society
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J. Physiol. Pharmacol. · Dec 1997
ReviewMechanisms of acute respiratory distress syndrome: role of surfactant changes and mechanical ventilation.
Acute respiratory distress syndrome (ARDS) is a condition characterized by a high permeability oedema due to loss of the integrity of the alveolo-capillary barrier with impairment of normal surfactant function, resulting in an increased collapse tendency of the alveoli. Mechanical ventilation on such alveoli with repeated alveolar collapse and subsequent reexpansion results in severe lung parenchymal injury and may induce further surfactant impairment. ⋯ Recent evidence from experimental studies has shown that ventilator modes which allow end-expiratory collapse can induce bacterial translocation from the lung into the bloodstream and trigger the release of inflammatory mediators, which can also be presented by maintaining end-expiratory alveolar volume. These data suggest that the interaction between surfactant changes and mechanical ventilation may play a role in the transition of ARDS into the systematic inflammatory disease process of multiple system organ failure (MSOF).
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J. Physiol. Pharmacol. · Dec 1997
ReviewPhysiologic, metabolic and mediator responses in posttrauma ARDS and sepsis: is oxygen debt a critical initiating factor?
Posttrauma adult respiratory distress syndrome (ARDS) and sepsis initiate complex humoral and cellular inflammatory responses that initially effect the microvascular system, but rapidly extend to involve and modulate the solid organ metabolic response. It is discussed whether the interaction between these cellular processes and the organs which they involve appear to be initiated by the trauma induced oxygen debt.
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The available data supporting the role of oxygen radicals (OR0) as fundamental--though not unique--mediators in the pathogenesis of sepsis and septic shock are reviewed. The main questions are 1) Are there any signs of OR0 overgeneration during sepsis and septic shock? 2) Are there any indirect signs of OR0 damage during sepsis and septic shock? 3) Does OR0 inactivation affect the evolution and severity of sepsis and septic shock? 4) May the pathophysiology of sepsis and septic shock be viewed as a consequence of OR0 overgeneration? All these questions might receive affirmative answers; thus the relationships of OR0 with other mediators of sepsis and septic shock are discussed. ⋯ There are also very close relationships with nitric oxide, another free radical. The data in favour of an antioxidant therapy of sepsis and septic shock in humans are too few to be conclusive.