The pathogenesis of neurogenic pulmonary edema has been debated for ma
ny years. Whether cardiogenic mechanisms and increased pulmonary vascu
lar pressures are primary or even necessary for the production of pulm
onary edema has been argued, We used postictal pulmonary edema to stud
y this problem in a sheep model of neurogenic pulmonary edema with bic
ucullin-induced status epilepticus. Seizure-induced increases in pulmo
nary vascular pressures were averted with a reservoir system to mainta
in left atrial pressure (LAP) and pulmonary artery pressure (PAP) at p
reseizure levels. No increase in lung lymph flow occurred during seizu
res, in contrast to the doubling of lung lymph flow that occurred duri
ng seizures when ictal pulmonary vascular hypertension was not blocked
. These data support a primary role of pulmonary vascular pressure inc
reases in the production of neurogenic pulmonary edema.