Impedance is a complex and comprehensive function of hemodynamics that can be measured in vivo and from which certain metrics, including input impedance (Z₀), first harmonic impedance (Z₁) and characteristic impedance (Z_C), can be calculated. According to lumped-parameter models of intact human lungs, Z₁ is proportional to proximal artery (PA) stiffness and Z_C is directly proportional to PA stiffness and inversely proportional to size. Our goal was to investigate how these metrics of impedance are related to PA stiffness in isolated mouse lungs.

Sinusoidal pressure-flow tests in isolated lungs and static pressure-diameter tests in isolated PAs from inbred mice were performed after exposure to zero days (CTL) or ten days of hypoxia (HPH). To normalize mean PA pressure in isolated lungs, measurements were taken with and without vasodilation (Y27632, 1X10⁻⁵ M).

In PAs, the incremental elastic modulus (E_inc) increased with HPH (P<0.05); no differences in size were significant. In lungs, Z₁ increased (P<0.0001) but Z_C decreased (P<0.05) with HPH while mean PA pressure (and Z₀) increased (P<0.0001). When measured at the same pressure (and Z₀), Z₁ returned toward CTL values (P=0.10 vs. CTL) but Z_C remained decreased (P<0.00001). Under these conditions, PAs were still stiffer than CTL (P<0.0005) and slightly but not significantly larger (P=0.051).

Overall, Z₁ was sensitive to pressure-induced dilation and strain-stiffening in PAs but Z_C was additionally sensitive to HPH-induced stiffening. In contrast to intact human lungs, our results suggest that in isolated mouse lungs Z_C is inversely proportional to PA stiffness.