Histopathological changes of pulmonary vascular remodeling in dogs affected with pulmonary hypertension secondary to degenerative mitral valve disease

Abstract

Introduction/objectivesPulmonary 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. AnimalsLung samples obtained from the carcasses of 19 older small-breed dogs (Control, n = 5; DMVD, n = 7; DMVD + PH, n = 7). Materials and methodsLung tissue sections were stained with hematoxylin and eosin, Masson's trichrome, and proliferating cell nuclear antigen (PCNA) immunohistochemistry. ResultsThe 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. ConclusionsMedial 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.