[abstract] NOVEL NITRIC OXIDE-MEDIATED BRAIN-LUNG INTERACTIONS IN HYPERBARIC OXYGEN TOXICITY

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[abstract] NOVEL NITRIC OXIDE-MEDIATED BRAIN-LUNG INTERACTIONS IN HYPERBARIC OXYGEN TOXICITY

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Title: [abstract] NOVEL NITRIC OXIDE-MEDIATED BRAIN-LUNG INTERACTIONS IN HYPERBARIC OXYGEN TOXICITY
Author: Demchenko, IT; Piantadosi, CA
Abstract: BACKGROUND: Hyperbaric oxygen (HBO2) can cause severe lung damage both by direct toxicity and associated with CNS O2 toxicity. We have tested the hypothesis that the onset of HBO2-induced seizures accelerates pulmonary damage by activation of NO-mediated neuronal pathways and CNS-driven central hemodynamic alterationMATERIALS AND METHODS: Awake or anesthetized SD rats were exposed to O2 at 3 or 5 ATA to the point of convulsion or EEG signs of CNS O2 toxicity. Brain and central hemodynamic (CBF, PO2, systemic arterial and venous blood pressure, right ventricular pressure, heart rate, cardiac output and pulmonary blood volume) were measured during HBO2 exposure along with ex vivo lung injury indices in control rats, post-vagotomy, and animals pre-treated with NO synthase inhibitors or alpha/beta adrenergic or cholinergic receptor blockers or agonists.RESULTS: Rats exposed to 3 and 5 ATA developed acute transpulmonary fluid and protein leakage and severe lung injury associated with CNS O2 toxicity. Our experimental interventions implicated one or more of three possible mechanisms of HBO2-induced acute pulmonary damage: (a) hyperbaric oxygen inactivates endothelial NO and increases in endothelin synthesis leading to systemic vasoconstriction and greatly elevated systemic vascular resistance; (b) hyperbaric oxygen decreases cardiac output by an increase in afterload, a reduction in left ventricular function and bradycardia through nNOS-mediated sympathetic and parasympathetic tone with differential effects on the left vs. the right heart; (c) an HBO2-induced right/left circulatory imbalance in cardiac output shifts blood from systemic to pulmonary circulations, thus exaggerating pulmonary hypertension and leading to acute pulmonary edema and hemorrhageCONCLUSIONS: We have developed evidence for a novel physiological mechanism in which it appears that nitric oxide derived from nNOS drives cardiogenic-hydrostatic lung injury by modulation of CNS-mediated adrenergic/cholinergic pathways.
Description: Undersea and Hyperbaric Medical Society, Inc. (http://www.uhms.org )
URI: http://archive.rubicon-foundation.org/3687
Date: 2006

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  • UHMS Meeting Abstracts
    This is a collection of the published abstracts from the Undersea and Hyperbaric Medical Society (UHMS) annual meetings.

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