Evaluation of pulmonary arteriolar lesions in rats induced by cigarette smoke exposure combined with Klebsiella infection
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1. Collaborative Innovation Center for Chinese Medicine and Respiratory Diseases Co-constructed by Henan Province and Education Ministry, Henan University of Chinese Medicine, Zhengzhou 450046, China. 2. Academy of Chinese Medicine Sciences, Henan University of Chinese Medicine, Zhengzhou 450046

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R-33

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    Abstract:

    Objective To analyze the morphological and structural changes to pulmonary arterioles in rats induced by smoke exposure combined with Klebsiella infection, and to evaluate the severity of the pulmonary arteriolar lesions. Methods Pulmonary arteriolar images from lung sections of control and model rats treated with smoke exposure combined with Klebsiella infection were analyzed by qualitative and quantitative method. Victorian-blue-stained sections were used for the detection of pulmonary arteriolar muscularization, vascular wall thickness, vascular occlusion score, the intima thickness and media thickness of muscular arterioles, and neointima proliferation. Hematoxylin and eosin-stained sections were used for the observation and detection of inflammatory cell infiltration and plexiform lesions around arterioles. Van Gieson-stained sections were used for the observation of collagen fibers in the intima and detection of the percentage of collagen fiber area in the arteriolar wall. Based on the above analyses, the degree of pulmonary arteriolar pathology was rated according to Heath-Edwards criteria. Results For ≤ 50 μm diameter arterioles, the percentage of non-muscular vessels was significantly decreased(P<0. 01) , the percentage of muscular vessels was increased(P<0. 01) , the percentage of partial muscular vessels was not significantly different(P>0. 05) , the thicknesses of the non-muscular vessel walls and muscular vessel walls were significantly increased(P<0. 05,P<0. 01) , and the occlusion scores of both non-muscular and muscular pulmonary arterioles were significantly increased in the model group compared with the Control group(P<0. 05,P<0. 01) . For 50 μmP<0. 05) , the percentages of muscular vessels and partial muscular vessels were not significantly different(P>0. 05) , the wall thickness and occlusion score of muscular vessels were significantly increased ( P<0. 05 ) , and the wall thickness and occlusion score of non-muscular vessels were not significantly different in the model group compared with the Control group (P>0. 05) . Compared with the Control group, the model group showed significantly increased intimal thickness and media thickness and significantly increased perivascular inflammatory infiltration score in both muscular arterioles of ≤ 50 μm diameter and 50 μmP<0. 05,P<0. 01) . In the Control group ( n= 9) , only one section with two neointimal lesions was found, and the degree of neointima proliferation was 1. 61%. In the model group ( n= 10) , five sections had neointima lesions, and the degree of neointima proliferation was 1. 04% to 17. 14%. No plexiform lesions were found in any section. For pulmonary arterioles with a 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 walls ( P>0. 05) . According to Heath-Edwards criteria, the pulmonary arteriole lesions in the model rats did not reach grade III. Conclusions The model rats showed pathological manifestations such as pulmonary arteriolar muscularization, thickening of the intima and media, and mild to moderate inflammatory reactions around arterioles. The low amount of neointimal proliferation and collagen fibers in the vascular wall and the absence of plexiform lesions suggest that the model may be up to grade II lesions, according to the Heath-Edwards criteria.

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History
  • Received:March 01,2024
  • Online: October 15,2024
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