Objective To study the reversal of pulmonary hypertension (PH) and associated haemodynamic and morphological pulmonary vascular changes caused by hypobaric hypoxia, once the hypoxic stimulus is ended.
Methods 50 Wistar rats (aged 8 weeks) were maintained for 28 days in a hypobaric chamber (Rec 0 group). After recovery in normoxia of 0, 1, 2, 4 and 6 weeks, respectively (Rec 1, Rec 2, Rec 4 and Rec 6 groups), they were killed per 10 animals. A control group of 10 rats was kept in room air at normal pressure for 28 days (control group).
Results Hypobaric hypoxia caused an increase in right ventricular systolic pressure (RVSP) (control group 14.7 ± 32.5 mm Hg, Rec 0 group: 73.8 ± 11.1 mm Hg; p<0.05). During recovery in normoxia RVSP decreased (Rec 6: 50.9 ± 16.8 mm Hg; p<0.05 compared with Rec 0). In pulmonary vessels of 50–150 μm, hypoxia caused a significant increase in both medial thickness (MT) and adventitial thickness (AT) (MT: control 18.3 ± 10.2%, Rec 0: 31.1 ± 9.9% (p<0.05), AT: control: 34.0 ± 9.9%, Rec 0: 44.7 ± 8.5 (p<0.05)). After 4–6 weeks of recovery MT and AT gradually decreased to values not significantly different from controls.
Conclusion Hypobaric hypoxia can induce PH in rats and causes morphometric lung vascular abnormalities. Regression of lung vascular abnormalities occurs once the hypoxic stimulus is ended. The underlying molecular pathophysiological pathways involved in regression of the morphometric lung vascular abnormalities in PH can now be studied.