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.