Background and Aims Catheter-related thrombosis (CRT) is one of the main complications of central venous catheterization. At present, the treatment of CRT is mainly based on anticoagulant and thrombolytic therapies. Clot dissolution is of great importance for restoring patency of the affected vessel, and directly affects the occurrence of post-thrombotic complications and the prognosis of patients. Studies have demonstrated that heme oxygenase 1 (HO-1) plays an important role in the process of thrombolysis and recanalization after the formation of deep venous thrombosis. However, its effects in CRT have rarely been reported. Therefore, this study was conducted to investigate the effect of HO-1 in clot dissolution and recanalization in rat model of CRT and the relevant mechanism, so as to provide new ideas and theoretical basis for clinical treatment of CRT.Methods A total of 72 healthy male SD rats aged 7-8 weeks underwent superior vena cava catheterization for 10 d to induce CRT models. Then, rats were equally randomized into model group, HO-1 agonist group and HO-1 inhibitor group. Rats in model control group did not receive any intervention, and those in the latter two groups received abdominal injection of HO-1 agonist cobalt protoporphyrin (CoPP) and inhibitor tin protoporphyrin (SnPP), respectively. Both treatment doses were 5 mg/kg. On the 1st, 7th, 14th and 28th d after that, 6 rats in each group were sacrificed, the blood was collected from the abdominal aorta, and the serum levels of HO-1, IL-6 and IL-10 were determined by ELISA assay; the affected vessels were harvested to observe the thrombolysis and calculate the thrombolysis rate by HE staining, to examine the expression of endothelial mark CD31 by immunohistochemical staining, and to detect the HO-1 mRNA expression by qPCR.Results The results of HE staining showed that thrombolysis was increased with time elapsed in each group, the thrombolysis rate was higher in HO-1 agonist group was lower in HO-1 inhibitor group than that in model group at each defined time point (all P<0.05), and on the 28th d, the vessels presented nearly complete recanalization in HO-1 agonist group, while only partial recanalization in HO-1 inhibitor group. The results of immunohistochemical staining showed that the expression of CD31 was higher in HO-1 agonist group and was lower in HO-1 inhibitor group than that in model group at each defined time point (all P<0.05). The results of ELISA assay showed that the serum levels of HO-1 and IL-10 were increased and the serum level of IL-6 was decreased in HO-1 agonist group compared with model group at each defined time point, while the opposite changes in these variables were observed in HO-1 inhibitor group (all P<0.05). The results of qPCR showed that the HO-1 mRNA expression in the vascular tissue in HO-1 agonist group was higher than that in model group at each defined time point, while the opposite view occurred in HO-1 inhibitor group (all P<0.05).Conclusion HO-1 can promote the clot dissolution and recanalization of CRT in rats, and its mechanism may be related to its inhibiting inflammatory response and promoting angiogenesis.