Abstract:Objective To analyze the morphological and structural changes of pulmonary arterioles in rats induced by smoke exposure combined with Klebsiella infection, and to evaluate the severity of pulmonary arteriolar lesions. Methods Pulmonary arteriolar images of lung sections of control rats and model rats induced by smoke exposure combined with Klebsiella infection were analyzed by qualitative and quantitative methods. Victorian blue stained sections were used for the detection of pulmonary arteriolar muscularization, vascular wall thickness, vascular occlusion score, intima thickness and media thickness of muscular arterioles, and neointima proliferation. HE stained sections were used for the observation and detection of inflammatory cell infiltration and plexiform lesions around arterioles. VG stained sections were used for the observation of collagen fibers in the intima and detection of the percentage of collagen fibers area in arteriolar wall area. Based on the above results, the degree of pulmonary arteriolar lesions was rated according to the Heath-Edwards criteria. Results For diameter ≤ 50 μm arterioles, compared with the control group, the percentage of non-muscular vessels was significantly decreased, the percentage of muscular vessels was increased, the percentage of partial muscular vessels was not significantly different, the wall thickness of non-muscular vessels and the wall thickness of muscular vessels were significantly increased, and the occlusion scores of both non-muscular and muscular pulmonary arterioles were significantly increased in the model group. For 50 < diameter ≤ 100 μm arterioles, compared with the control group, the percentage of non-muscular vessels was significantly decreased, the percentage of muscular vessels and the percentage of partial muscular vessels were not significantly different, the wall thickness and occlusion score of muscular vessels were significantly increased, the wall thickness and occlusion score of non-muscular vessels were not significantly different in the model group. Compared with the control group, the intimal thickness and media thickness were significantly increased and the perivascular inflammatory infiltration score was significantly increased in muscular arterioles with both diameter of ≤ 50 μm and 50 < diameter ≤ 100 μm of the model group. In the control group (n=9), only one section with neointimal lesion was found with 1.61 % of proliferation degree of neointima. In the model group (n=10), five sections had neointima lesion from 1.04 % to 17.14 % of proliferation degree of neointima, respectively. No plexiform lesions were found in a11 sections. For pulmonary arterioles with diameter of ≤ 100 μm, there was no change in the expression of intimal collagen fibers in the model group compared with the control group, and there was no significant difference in the percentage of collagen fiber area in the vessel wall area. According to the Heath-Edwards criteria, the pulmonary arteriole lesions in the model rats did not reach grade III. Conclusions The model rats show pathological manifestations such as pulmonary arteriolar muscularization, thicking intima and media, and mild to moderate inflammatory reactions around arterioles. The low degree of neointimal proliferation and collagen fiber in the vascular wall and no plexiform lesions suggest that the model is up to grade II lesion according to the Heath-Edwards criteria.