Although many recently produced transgenic mice possess gene alterations af
fecting pulmonary vascular function, there are few baseline measurements of
vascular resistance and permeability. Therefore, we excised the lungs of C
57/BL6 mice and perfused them with 5% bovine serum albumin in RPMI-1640 cul
ture medium at a nominal flow of 0.5 ml/min and ventilated them with 20% O-
2-5% CO2-75% N-2. The capillary filtration coefficient, a sensitive measure
ment of hydraulic conductivity, was unchanged over 2 h (0.33 +/- 0.03 ml .
min(-1) . cmH(2)O(-1) . 100 g(-1)) in a control group ventilated with low p
eak inflation pressures (PIP) but increased 4.3-fold after high PIP injury.
Baseline pulmonary vascular resistance was 6.1 +/- 0.4 cmH(2)O . ml(-1) .
min . 100 g(-1) and was distributed 34% in large arteries, 18% in small art
eries, 14% in small veins, and 34% in large veins on the basis of vascular
occlusion pressures. Baseline vascular compliance was 5.4 +/- 0.3 ml . cmH(
2)O(-1) . 100 g(-1) and decreased significantly with increased vascular pre
ssures. Baseline pulmonary vascular resistance was inversely related to bot
h perfusate flow and microvascular pressure and increased to 202% of baseli
ne after infusion of 10(-4) M phenylephrine due to constriction of large ar
terial and venous segments. Thus isolated mouse lung vascular permeability,
vascular resistance, and the longitudinal distribution of vascular resista
nce are similar to those in other species and respond in a predictable mann
er to microvascular injury and a vasoconstrictor agent.