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Long-term administration of prednisolone: Effects on the myocardial tissue of healthy beagle dogs

Authors
  • TANAKA, Sachiyo1
  • SHIBUYA, Hitomi1
  • SUZUKI, Shuji1
  • KANNO, Nobuo1
  • HARADA, Yasuji1
  • SATO, Asaka2
  • SOETA, Satoshi3
  • HARA, Yasushi1
  • 1 Division of Veterinary Surgery, Department of Veterinary Science, Faculty of Veterinary Medicine, Nippon Veterinary and Life Science University, 1-7-1 Kyonan, Musashino, Tokyo 180-8602, Japan
  • 2 Azabu University Veterinary Teaching Hospital, Soft Tissue and Tumor Surgery, 1-17-71 Fuchinobe, Chuo, Sagamihara, Kanagawa 252-5201, Japan
  • 3 Division of Veterinary Anatomy, Department of Veterinary Science, Faculty of Veterinary Medicine, Nippon Veterinary and Life Science University, 1-7-1 Kyonan, Musashino, Tokyo 180-8602, Japan
Type
Published Article
Journal
The Journal of Veterinary Medical Science
Publisher
The Japanese Society of Veterinary Science
Publication Date
Dec 02, 2020
Volume
83
Issue
1
Pages
84–93
Identifiers
DOI: 10.1292/jvms.20-0401
PMID: 33268642
PMCID: PMC7870400
Source
PubMed Central
Keywords
License
Green

Abstract

This study aimed to assess the structural and functional effects of long-term hyperglucocorticoidemia on canine myocardium and compare these parameters with histopathological changes. Twelve healthy male beagle dogs were enrolled and assigned to the high-dose prednisolone (P; n=6) and control (C; n=6) groups. The P group was treated with 2 mg/kg of prednisolone BID for 84 days. Clinical parameters were measured using echocardiography and non-invasive systolic blood pressure (SBP) measured before the initiation of synthetic corticosteroids and at 7, 28, 56, and 84 days after the start of medication. For histological evaluation, cardiovascular tissue was harvested from dogs in groups P (at the end of the medication period) and C (scheduled to be euthanized for unrelated reasons). In the P group, clinical changes including thickening of the left ventricular free wall (LVFW) and interventricular septum (IVS), decreased left ventricular (LV) diastolic function, and increased SBP were observed after the start of medication. During histological evaluation, fibrosis was observed in the LVFW and IVS in the P group. Furthermore, decreased glucocorticoid receptor (GCR) levels were observed in the LVFW, right ventricular free wall (RVFW), and IVS and increased mineralocorticoid receptor (MCR) levels were observed in the LVFW and RVFW in the P group compared with those in the C group. In conclusion, fibrosis may cause LV structural and functional abnormalities in dogs with hyperadrenocorticism. Furthermore, GCR downregulation and upregulated MCR might influence the myocardial fibrosis.

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