Pulmonary hypertension and cor pulmonale are complications of severe equine asthma, as a consequence of pulmonary hypoxic vasoconstriction. However, as pulmonary hypertension is only partially reversible by oxygen administration, other etiological factors are likely involved. In human chronic obstructive pulmonary disease, pulmonary artery remodeling contributes to the development of pulmonary hypertension. In rodent models, pulmonary vascular remodeling is present as a consequence of allergic airway inflammation. The present study investigated the presence of remodeling of the pulmonary arteries in severe equine asthma, its distribution throughout the lungs, and its reversibility following long-term antigen avoidance strategies and inhaled corticosteroid administration. Using histomorphometry, the total wall area of pulmonary arteries from different regions of the lung of asthmatic horses and controls was measured. The smooth muscle mass of pulmonary arteries was also estimated on lung sections stained for α-smooth muscle actin. Reversibility of vascular changes in asthmatic horses was assessed after 1 year of antigen avoidance alone or treatment with inhaled fluticasone. Pulmonary arteries showed increased wall area in apical and caudodorsal lung regions of asthmatic horses in both exacerbation and remission. The pulmonary arteries smooth muscle mass was similarly increased. Both treatments reversed the increase in wall area. However, normalization of the vascular smooth muscle mass was observed only after treatment with antigen avoidance, but not with fluticasone. In conclusion, severe equine asthma is associated with remodeling of the pulmonary arteries consisting in an increased smooth muscle mass. The resulting narrowing of the artery lumen could enhance hypoxic vasoconstriction, contributing to pulmonary hypertension. Vascular smooth muscle mass normalization is better achieved by antigen avoidance than with inhaled corticosteroids.

中文翻译：

---

严重哮喘与马肺动脉重塑有关

肺动脉高压和肺心病是由于肺缺氧性血管收缩而导致的严重马哮喘的并发症。然而，由于肺动脉高压只能通过氧疗部分逆转，因此可能涉及其他病因。在人类慢性阻塞性肺疾病中，肺动脉重构有助于肺动脉高压的发展。在啮齿动物模型中，由于过敏性气道炎症而导致肺血管重塑。本研究调查了严重马哮喘中肺动脉重塑的存在，其在整个肺中的分布以及长期的抗原回避策略和吸入皮质类固醇给药后的可逆性。使用组织形态计量学 测量了哮喘马匹和对照组肺不同区域的肺动脉总壁面积。在α-平滑肌肌动蛋白染色的肺切片上也估计了肺动脉的平滑肌质量。单独避开抗原1年或吸入氟替卡松治疗1年后，评估哮喘马的血管变化的可逆性。在急性期和缓解期中，哮喘马的心尖和尾鼻肺区的肺动脉壁面积增加。肺动脉平滑肌质量同样增加。两种处理都可以逆转壁面积的增加。但是，只有在避免使用抗原后才观察到血管平滑肌质量正常化，而未用氟替卡松治疗后才观察到。结论，严重的马哮喘与肺动脉重塑有关，包括平滑肌质量增加。导致的动脉管腔变窄可能会增强缺氧性血管收缩，导致肺动脉高压。与吸入皮质类固醇激素相比，通过避免抗原可以更好地实现血管平滑肌质量正常化。