Induction of non‐cardiogenic pulmonary edema following cerebral hypoxia in a canine model

Abstract

Neurogenic pulmonary edema (NPE) is a non‐cardiogenic pulmonary edema associated with stroke, traumatic brain injury and seizure with high morbidity and mortality, yet the underlying mechanism(s) is unknown.HypothesisWe hypothesize that cerebral hypoxemia induces pulmonary edema in the presence of systemic normoxia.MethodsUsing an updated Moss's model for induction of cerebral hypoxia, 8 Walker hounds (25–30kg) were randomly assigned into cerebral hypoxemia (SaO2 ~55%) with systemic normoxia (SaO2 ~90%) (CH; n=4), cerebral and systemic hypoxemia (SaO2 ~ 50%) (GH; n=2), and cerebral and systemic normoxia (SaO2 ~90%) (Con; n=2). In this model, femoral venous (hypoxic) or arterial (normoxic) perfusate was delivered from a cardiopulmonary bypass circuit to the brain. Outcomes included the wet to dry lung weight ratio as an index of pulmonary edema, hemodynamic measurements, intracranial pressure (ICP) and cerebral blood flow.ResultsWet to dry weight ratio was increased in the CH and GH groups compared to control. We observed no changes in hemodynamic parameters in CH dogs, with the exception of an increase in ICP. Dogs with GH exhibited increased cardiac output, pulmonary artery pressure and cerebral blood flow, with decreased systemic blood pressures; no increase in ICP was observed.ConclusionBrain hypoxemia, in the absence of systemic hypoxemia, induces pulmonary edema in this canine model. DARPA N66001‐10‐C‐2134.