We designed a series of experiments to compare the pulmonary dysfuncti
on observed in models of cardiogenic and noncardiogenic pulmonary edem
a in chronically instrumented awake sheep. Cardiogenic pulmonary edema
was induced by inflating the balloon of a Foley catheter surgically p
ositioned in the mitral valve orifice causing increased left atrial pr
essure (up arrow PLA). Noncardiogenic pulmonary edema was induced by i
ntravenous infusion of Perilla ketone (PK). Calculated microvascular p
ressure remained constant during PK infusion but increased from 9.4+/-
0.7 to 42.8+/-2.4 cm H2O during up arrow PLA. Comparable increases in
lung lymph flow (QL) were observed in the two protocols (five to seven
times baseline). Pulmonary edema as quantified by chest radiograph sc
ores increased from 0 (normal) to 2.9+/-0.5 and 3.6+/-0.1 in the PK an
d up arrow PLA groups, respectively. Room air alveolar to arterial oxy
gen pressure difference (P[A-a]O-2) increased from 24+/-3 to 46+/-7 mm
Hg in the PK group and from 23+/-4 to 56+/-6 mm Hg in the up arrow PL
A group. Dynamic compliance of the lungs (Cdyn) expressed as the perce
ntage of the baseline value decreased to 53 +/- 7 and 50 +/- 7% in the
PK and up arrow PLA groups, respectively. Resistance to airflow acros
s the lungs (RL) increased from 2.5+/-0.6 to 3.3+/-0.8 cm H2O . L(-1).
sec(-1) in the PK group and from 1.4+/-0.3 to 4.2+/-1.1 in the up arr
ow PLA group. Significant correlations were observed between changes i
n the severity of pulmonary edema observed on chest radiographs, Cdyn,
Delta P(A-a)O-2, and QL in both the up arrow PLA groups. We conclude
that similar degrees of pulmonary edema, regardless of the mechanism,
are associated with similar changes in QL, Cdyn, and Delta P(A-a)O-2.
Hydrostatic pulmonary edema appeared to cause greater changes in RL th
an that resulting from increased microvascular permeability.