Abstract: AIM To investigate the effects of Kawasaki disease (KD) on pulmonary vascular endothelial function and to evaluate any correlation with pulmonary hypertension. METHODS Forty rats (1 month old) were randomly divided into a control group and a KD group. The rats in the KD group were intraperitoneally injected with lactobacillus casei cell wall extract (LCWE) 0.5 ml (1 mg/ml). Two weeks after modeling, coronary artery and pulmonary artery injury were histopathologically assessed. Blood pressure, right ventricular pressure, right ventricular hypertrophy index and pulmonary artery diastolic function were measured. The levels of antioxidant enzymes MnSOD, Catalase and oxidative stress were measured in pulmonary arterioles. RESULTS After 14 days of LCWE injection, coronary artery injury in the KD rats was successfully induced (P<0.05). On this basis, it was demonstrated that KD rats had lung injury, pulmonary edema, point/flaky hemorrhage, and neutrophil-like inflammatory cell infiltration. Pulmonary arterial endothelial cells were swollen, irregular intermittent hypertrophy appeared in the middle layer, and the lumen was partially narrowed and the pulmonary artery injury score increased (P<0.05). It was revealed that levels of MnSOD and Catalase in pulmonary arterioles were significantly lower than those in the control group (P<0.05), while levels of MPO and MDA in oxidative stress were significantly increased (P<0.05). The right ventricular pressure and hypertrophy index of the KD rats were significantly increased (P<0.05). In vitro vascular perfusion experiments confirmed that pulmonary arterial endothelium-dependent relaxation effect was significantly reduced in KD rats (P<0.01). CONCLUSION In addition to known coronary damaging effects, Kawasaki disease can lead to pulmonary arteritis, causing pulmonary arterial vascular injury and oxidative stress injury, which may potentially induce pulmonary hypertension and secondary heart injury.