Abstract
Neurogenic pulmonary edema (NPE) is a life-threatening complication of central nervous system (CNS) injuries. This review summarizes current knowledge about NPE etiology and pathophysiology with an emphasis on its experimental models, including our spinal cord compression model.
NPE may develop as a result of activation of specific CNS trigger zones located in the brainstem, leading to a rapid sympathetic discharge, rise in systemic blood pressure, baroreflex-induced bradycardia, and enhanced venous return resulting in pulmonary vascular congestion characterized by interstitial edema, intra-alveolar accumulation of transudate, and intra-alveolar hemorrhages. The potential etiological role of neurotransmitter changes in NPE trigger zones leading to enhanced sympathetic nerve activity is discussed.
Degree of anesthesia is a crucial determinant for the extent of NPE development in experimental models because of its influence on sympathetic nervous system activity. Sympathetic hyperactivity is based on the major activation of either ascending spinal pathways by spinal cord injury or NPE trigger zones by increased intracranial pressure.
Attenuation of sympathetic nerve activity or abolition of reflex bradycardia completely prevent NPE development in our experimental model. Suggestions for future research into NPE pathogenesis as well as therapeutic potential of particular drugs and interventions are discussed.