Resolution of pulmonary hypertension and other features induced by chronic hypoxia in rats during complete and intermittent normoxia.

Rats subjected to 10% O2 (hypoxic rats) for various periods and recovery regimens were compared with control animals with respect to pulmonary artery pressure (Ppa), right ventricular hypertrophy (RVH), and muscularisation of small pulmonary vessels. Mean Ppa was measured in anaesthetised animals spontaneously breathing air and rose from 16 mmHg in controls to 36 mmHg in rats exposed to hypoxia for three weeks. Ppa had returned to normal after 20 weeks' recovery in air. RVH regressed a little more quickly, but muscularisation of small pulmonary vessels. Mean Ppa was measured in anaesthetised animals spontaneously breathing air and rose from 16 mmHg in controls to 36 mmHg in rats exposed to hypoxia for three weeks. Ppa had returned to normal after 20 weeks' recovery in air. RVH regressed a little more quickly, but muscularisation of small pulmonary vessels was still apparent after 20 weeks. Some hypoxic rats were subjected to an intermittent normoxic recovery regimen for either 40 or 80 hours a week in air, the remainder in 10% O2. Some reduction in RVH probably occurred after six weeks on the 80-hour regimen, but there was no reduction in Ppa or muscularisation of small pulmonary vessels. These results suggest that the pulmonary hypertension of chronic alveolar hypoxia resolves very slowly and is probably related to structural changes in the pulmonary vessels. Their relevance to human cor pulmonale and intermittent long-term oxygen treatment for these patients is discussed.