Analysis of airway fluid protein concentration in neurogenic pulmonary edema

Abstract

Intracisternal administration of veratrine (40 micrograms/kg) in the alpha-chloralose-anesthetized dog produces fulminant neurogenic pulmonary edema (NPE). To determine whether the edema resulted from increased microvascular pressure or from increased permeability, the airway fluid-to-plasma protein (A/P) concentration ratios were compared for both total proteins and endogenous protein fractions of known molecular radii (37-114 A) from dogs with edema produced by either veratrine, alloxan (permeability edema), or combined left atrial pressure and volume overload (hemodynamic edema). High A/P ratios (0.98 +/- 0.05) were observed after alloxan administration, whereas lower values (0.54 +/- 0.04) were observed in hemodynamic edema. A/P ratios were observed after veratrine administration that formed a continuum (0.48-0.84) between these extremes. Veratrine animals with high overall A/P ratios exhibited elevated A/P ratios for all protein fractions, whereas animals with lower overall A/P ratios exhibited A/P protein fraction ratios similar to those observed in the hemodynamic group. These data indicate that both hemodynamic and increased permeability mechanisms may play a role to varying degrees in the development of this form of NPE.