Objective: To investigate whether succinic acid could exacerbate the early interstitial fibrosis of cardio-pulmonary arteries induced by monocrotaline in a rat model of pulmonary hypertension, and to explore its pathological and molecular mechanisms. Methods: A total of 30 healthy male SD rats aged 4 to 5 weeks and weighted 120~180 g were randomly divided into the control group(C group), the monocrotaline group(MCT group), and the monocrotaline and succinic acid group(MCT+SUC group), with 10 rats in each group. The MCT group and the MCT+SUC group were subjected to intraperitoneal injection with monocrotaline in 60 mg/kg. The MCT+SUC group was given SUC for 4 weeks. The rats in the control group and the MCT group were injected with equal volume of saline, lasting for 4 weeks. After 4 weeks, hemodynamic indices including mean pressure of pulmonary artery(mPAP), right ventricular systolic pressure(RVSP), systolic blood pressure(SBP) and diastolic blood pressure(DBP) of pulmonary artery were measured by floating catheter in all groups. The right ventricular hypertrophy index was measured after euthanasia. HE staining, Masson staining and Sirius red staining were conducted to detect the remodeling of arteriole in the heart and lung tissues. Western blot and immunohistochemistry were conducted to examine the protein level of angiotensinⅡ(AngⅡ), platelet derived growth factor(PDGF-BB), and platelet derived growth factor(FGF2) in the pulmonary hypertension rat model. Results： The rats in the MCT group and the SUC group both showed decreased activity, sleepiness and poor appetite. Lips cyanosis and shortness of breath appeared earlier in the MCT+SUC group. Hemodynamic examination exhibited that indices, including mPAP, RVSP, SBP and DBP of pulmonary artery, the right ventricular hypertrophy index, the thickening of arteriole in the heart and lung tissues were significantly higher in the MCT+SUC group than those in the MCT group(all P<0.05). HE staining showed slight thickening of the small arteries in the MCT group, the degree of thickening of the arterial wall of the MCT+SUC group was more obvious than that of the MCT group, and the infiltration of inflammatory cells in local myocardium increased. Sirius red staining and Masson staining showed abnormal proliferation of collagen fibers in the interstitial cells of the MCT+SUC group, and no abnormal collagen fibers in the MCT group. Western blot and immunohistochemistry showed that AngⅡ, FGF-2 and PDGF-BB expression levels in the MCT+SUC group and the MCT group were significantly higher than those in the control group, and the protein expressions of AngⅡ, FGF-2 and PDGF-BB in the MCT+SUC group increased more significantly than those in the MCT group. Conclusion: Succinic acid can exacerbate the formation of early fibrosis of cardiopulmonary arterioles in rats with pulmonary hypertension induced by monocrotaline. The mechanism may be due to regulating the expression of FGF-2 and PDGF-BB in the body, and eventually lead to increased expression of AngⅡ, causing interstitial fibrosis of cardio-pulmonary arteries.