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Departments of 1 Physiology and 2 Pharmacology, University of South Alabama, Mobile, Alabama 36688
Although many recently produced transgenic mice
possess gene alterations affecting pulmonary vascular function, there
are few baseline measurements of vascular resistance and permeability. Therefore, we excised the lungs of C57/BL6 mice and perfused them with
5% bovine serum albumin in RPMI-1640 culture medium at a nominal flow
of 0.5 ml/min and ventilated them with 20%
O2-5% CO2-75%
N2. The capillary filtration
coefficient, a sensitive measurement of hydraulic conductivity, was
unchanged over 2 h (0.33 ± 0.03 ml · min
1 · cmH2O
1 · 100 g
1) in a control group
ventilated with low peak inflation pressures (PIP) but increased
4.3-fold after high PIP injury. Baseline pulmonary vascular resistance
was 6.1 ± 0.4 cmH2O · ml
1 · min · 100 g
1 and was distributed 34%
in large arteries, 18% in small arteries, 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 · cmH2O
1 · 100 g
1 and decreased
significantly with increased vascular pressures. Baseline pulmonary
vascular resistance was inversely related to both perfusate flow and
microvascular pressure and increased to 202% of baseline after
infusion of 10
4 M
phenylephrine due to constriction of large arterial and venous segments. Thus isolated mouse lung vascular permeability, vascular resistance, and the longitudinal distribution of vascular resistance are similar to those in other species and respond in a predictable manner to microvascular injury and a vasoconstrictor agent.
vasoconstriction; pulmonary edema; mechanical stress failure; capillary filtration coefficient; transgenic mice
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