Objective To evaluate pulmonary vascular remodeling, right ventricular function, intestinal barrier integrity, and inflammatory factor expression in rat models of pulmonary hypertension (PH) induced by normobaric and hypobaric hypoxia. Additionally, to compare modeling methods and establish an experimental basis for understanding PH pathogenesis and developing treatment strategies. Methods Method: From June to December 2024, eighteen 6-week-old male SPF SD rats were randomly assigned to three groups: normobaric normoxia (Control), normobaric hypoxia (NH), and hypobaric hypoxia (HH). Mean pulmonary artery pressure (mPAP) was measured by right heart catheterization. Right ventricular function was assessed using echocardiography and the right ventricular hypertrophy index. Pulmonary vascular remodeling and intestinal mucosal barrier damage were evaluated via hematoxylin-eosin (HE) staining. Colon permeability was quantified by colon ligation followed by FITC-dextran injection. The expression levels of inflammatory factors in lung and colon tissues were analyzed using enzyme-linked immunosorbent assay (ELISA). Results Right heart function assessment revealed that, compared with group C, rats in groups NH and HH exhibited significantly increased mPAP (P < 0.05), shortened PAAT, and elevated RVHI and RVFWI (P < 0.05). Compared with group HH, rats in group NH demonstrated prolonged PET and a reduced PAAT/PET ratio, indicating more pronounced right heart dysfunction in group NH. Pulmonary vascular morphology analysis demonstrated that, compared with group C, WA% and WT% of pulmonary vessels were significantly higher in groups NH and HH (P < 0.05). Moreover, WA% was markedly increased in group NH relative to group HH (P < 0.05), suggesting more severe pulmonary vascular remodeling in group NH. Intestinal injury evaluation indicated that, compared with group C, rats in groups NH and HH exhibited shortened colon length, mucosal damage, and significantly increased permeability (P < 0.05). Group HH showed more prominent inflammatory cell infiltration compared with group NH, confirming intestinal mucosal barrier damage in both groups. Inflammation assessment of lung and colon tissues revealed that, compared with group C, the expression levels of IL6, IL1β, and IL17a were significantly elevated in lung and colon tissues of rats in groups NH and HH (P < 0.05). Notably, compared with group HH, group NH exhibited significantly higher expression of IL6 and IL1β in lung tissue and IL17a in colon tissue (P < 0.05), while IL6 expression in colon tissue was relatively lower (P < 0.05), indicating local inflammation in lung and colon tissues in both groups. Conclusions Phenotypic differences were identified between the two hypoxia-induced PH rat models, NH and HH, with respect to pulmonary vascular remodeling, right heart function, intestinal mucosal barrier injury, and the expression of inflammatory factors in lung and intestinal tissues. Additionally, our results demonstrate that variations in air pressure significantly contribute to the pathogenesis and progression of PH. Different air pressures may affect the development of PH via distinct mechanisms, thereby offering critical insights for further investigation into the pathological changes of PH, potential therapeutic strategies to mitigate disease progression, and the elucidation of inflammatory mechanisms underlying PH based on the "lung-intestine axis."