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. 2010 Feb 19;298(5):H1518–H1528. doi: 10.1152/ajpheart.00813.2009

Fig. 1.

Fig. 1.

Chronic hypoxia (CH) results in higher right ventricular (RV) pressures, and mitogen-activated protein (MAP) kinase phosphatase-1 (MKP)-1-deficient animals had higher RV pressures after chronic hypoxia than did wild-type (WT) animals. A: RV systolic pressures (RVSP) during 5 min of normoxia (black bars, FiO2 0.21), followed by 10 min of hypoxic (gray bars, FiO2 0.12), ventilation in anesthetized mice. Control animals were exposed to room air, whereas CH animals were exposed to hypobaric hypoxia (barometric pressure ≈ 380 mmHg) for 4 wk before study. Both WT and Mkp-1−/− [knockout (KO)] mice were studied. There were 5 animals in each study group, except for the CH KO, which had 4 animals. P < 0.05, hypoxic ventilation different from normoxic ventilation in the anesthetized animals in the same group (*), chronic hypoxia-exposed animals different from control animals in the same genotype and ventilation (#), and CH KO animals different from CH WT animals in the same ventilation condition ($). B: RV diastolic pressures from the same animals as in A. There were no differences in diastolic pressures with either ventilation, exposure, or genotype.