Fig. 6: AMPK-α1/α2 deletion increased pulmonary vascular resistance and attenuated hypoxic pulmonary vasoconstriction after birth.
a i-ii Upper panels show representative spectral Doppler peak systolic velocities versus time within the main pulmonary artery of (i) AMPK-α1/α2 floxed (FLX) and (ii) AMPK-α1/α2 KO mice during normoxia, hypoxia (8% O2) and recovery; lower panels show example records of Doppler velocity during normoxia, hypoxia (shaded green) and recovery. Scatter plots show the mean ± SEM for the (iii) basal peak velocity under normoxia for AMPK-α1/α2 FLX (n = 13 mice) and AMPK-α1/α2 KO (n = 10 mice) and (iv) the maximum change in peak velocity observed during 8% O2 for AMPK-α1/α2 FLX (n = 7 mice) and AMPK-α1/α2 KO mice (n = 4 mice). b Graphs illustrate age-dependent changes in right ventricular systolic (S) and diastolic (D) pressures for (i) AMPK-α1/α2 floxed and (ii) AMPK-α1/α2 KO mice (different weeks identified by different shades of gray). Scatter plots show values of right ventricular (iii) systolic and (iv) diastolic pressures for AMPK-α1/α2 FLX (n = 9) and AMPK-α1/α2 KO (n = 5). c Representative images of lung slices stained with Hematoxylin–Eosin, showing an intralobar artery (left), medium sized pulmonary artery (middle) and arteriole (right) for (i) AMPK-α1/α2 FLX (n = 9) and (ii) AMPK-α1/α2 KO euthanised at ~80 days (n = 5). Data are expressed as mean ± SEM and statistical significance was assessed by two- sided unpaired Student’s t test (aiii) and two- sided unpaired Mann–Whitney’s test (aiv, biii-iv).
