Pneumonectomized rats develop pulmonary hypertension (PH) and pulmonary vascular neointimal formation 4 wk after monocrotaline (MCT) administration. Male Sprague-Dawley rats were injected with MCT (60 mg/kg) on Day 7 after left pneumonectomy. Three groups (n = 5) received 40-O-(2-hydroxyethyl)-rapamycin (RAD, 2.5 mg/kg/d, by gavage): Group PMR_5–35 from Day 5 to Day 35, Group PMR_5–14 from Day 5 to Day 14, and Group PMR_15–35 from Day 15 to Day 35. By Day 35, rats that received vehicle had higher mean pulmonary arterial pressures (Ppa = 41 ± 3 mm Hg) (p < 0.001), right ventricular systolic pressures (Prv,s = 45 ± 2 mm Hg) (p < 0.01), and right ventricle/(left ventricle plus septum) (0.55 ± 0.05) (p = 0.028) than rats in Groups PMR_5–35 (Ppa = 25 ± 3 mm Hg, Prv,s = 32 ± 7 mm Hg, RV/LV&S = 0.42 ± 0.06) and PMR_5–14 (Ppa = 29 ± 4 mm Hg, Prv,s = 30 ± 5 mm Hg, RV/LV&S = 0.43 ± 0.07). Pulmonary arterial neointimal formation (quantified by a vascular occlusion score) was more severe in vehicle-treated rats (1.93 ± 0.03) than in Groups PMR_5–14 (1.56 ± 0.27) and PMR_5–35 (1.57 ± 0.1) (p < 0.01). RAD attenuates the development of MCT-induced pulmonary arterial hypertension in the pneumonectomized rat.