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Histopathological changes of pulmonary vascular remodeling in dogs affected with pulmonary hypertension secondary to degenerative mitral valve disease
Journal of Veterinary Cardiology ( IF 1.5 ) Pub Date : 2021-06-24 , DOI: 10.1016/j.jvc.2021.06.005
S Sakarin 1 , A Rungsipipat 2 , S D Surachetpong 1
Affiliation  

Introduction/objectives

Pulmonary hypertension (PH) can cause pulmonary arterial remodeling. Medial remodeling is a structural change of the pulmonary artery seen with PH. Hyperplasia and hypertrophy of pulmonary arterial smooth muscle cells (SMCs) are suggested as causes of medial remodeling. To demonstrate the histopathological changes of the pulmonary artery in dogs affected with PH secondary to degenerative mitral valve disease (DMVD) compared with DMVD without PH and control dogs.

Animals

Lung samples obtained from the carcasses of 19 older small-breed dogs (Control, n = 5; DMVD, n = 7; DMVD + PH, n = 7).

Materials and methods

Lung tissue sections were stained with hematoxylin and eosin, Masson's trichrome, and proliferating cell nuclear antigen (PCNA) immunohistochemistry.

Results

The internal diameters of the pulmonary artery in the three groups were not different. Masson's trichrome staining revealed no collagen deposition in the intimal layer of the pulmonary artery in all dogs. The external diameter, percentage of medial thickness (%MT), percentage of SMC layer and collagen deposition areas, average number of SMCs, and the percentage of PCNA positive cells (%PCNA) of the pulmonary artery were increased in the DMVD and DMVD + PH groups compared with the control group. The %PCNA in the DMVD + PH group was significantly decreased when compared with the DMVD group.

Conclusions

Medial remodeling was found in left-sided heart failure DMVD dogs with and without PH. The medial remodeling in DMVD dogs with and without PH is related to SMC hyperplasia, hypertrophy, and collagen deposition, leading to an increased medial layer thickness of the pulmonary artery.



中文翻译:

退行性二尖瓣疾病继发肺动脉高压犬肺血管重构的组织病理学变化

介绍/目标

肺动脉高压 (PH) 可导致肺动脉重塑。内侧重塑是肺动脉的结构变化,可见于 PH。肺动脉平滑肌细胞 (SMC) 的增生和肥大被认为是内侧重塑的原因。证明与没有 PH 的 DMVD 和对照狗相比,继发于退行性二尖瓣疾病 (DMVD) 的 PH 影响的狗的肺动脉的组织病理学变化。

动物

从 19 只老年小型犬的尸体中获得的肺样本(对照,n = 5;DMVD,n = 7;DMVD + PH,n = 7)。

材料和方法

肺组织切片用苏木精和伊红、马森三色染色和增殖细胞核抗原 (PCNA) 免疫组织化学染色。

结果

三组肺动脉内径无差异。Masson 的三色染色显示所有狗的肺动脉内膜层都没有胶原蛋白沉积。DMVD和DMVD+肺动脉外径、中层厚度百分比(%MT)、SMC层百分比和胶原沉积面积百分比、SMC平均数、PCNA阳性细胞百分比(%PCNA)增加PH组与对照组比较。与 DMVD 组相比,DMVD + PH 组的 %PCNA 显着降低。

结论

在有和没有 PH 的左侧心力衰竭 DMVD 犬中发现了内侧重塑。有和没有 PH 的 DMVD 犬的内侧重塑与 SMC 增生、肥大和胶原沉积有关,导致肺动脉内侧层厚度增加。

更新日期:2021-07-18
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