Adjuvant-induced arthritis is a relevant model to mimic coronary and myocardial impairments in rheumatoid arthritis
Affiliation auteurs | !!!! Error affiliation !!!! |
Titre | Adjuvant-induced arthritis is a relevant model to mimic coronary and myocardial impairments in rheumatoid arthritis |
Type de publication | Journal Article |
Year of Publication | 2021 |
Auteurs | Bordy R, Moretto J, Devaux S, Wendling D, Moretto-Riedweg K, Demougeot C, Totoson P |
Journal | JOINT BONE SPINE |
Volume | 88 |
Pagination | 105069 |
Date Published | JAN |
Type of Article | Article |
ISSN | 1297-319X |
Mots-clés | adjuvant-induced arthritis, Coronary dysfunction, Heart dysfunction, Ischemia/reperfusion |
Résumé | Objectives: To determine if the adjuvant-induced arthritis model reproduced coronary and cardiac impairments observed in rheumatoid arthritis patients. The link between disease activity and circulating levels of angiotensin II and endothelin-1 have been studied, as well as the myocardial susceptibility to ischemia. Methods: At the acute inflammatory phase, coronary reactivity was assessed in isolated arteries, and cardiac function was studied in isolated perfused hearts, before and after global ischemia/reperfusion. Ischemic insult was evaluated by the infarct size, lactate dehydrogenase and creatine phosphokinase levels in coronary effluents. Cardiac myeloperoxidase activity was measured, as well as angiotensin II and endothelin-1 levels. Results: Compared to controls, adjuvant-induced arthritis had reduced coronary Acetylcholine-induced relaxation associated with cardiac hypertrophy, both being correlated with plasma levels of endothelin-1 and angiotensin II, and arthritis score. Although cardiac function at baseline was similar from controls, adjuvant-induced arthritis rats exhibited lower cardiac functional recovery, increased myeloperoxidase activity, higher infarct size and creatine phosphokinase levels after ischemia/reperfusion. Conclusions: The adjuvant-induced arthritis model displays coronary endothelial dysfunction associated with myocardial hypertrophy and a reduced tolerance to ischemia. This model might be useful for deciphering the pathophysiology of cardiac dysfunction in rheumatoid arthritis and paves the way for studying the role of endothelin-1 and angiotensin II. (C) 2020 Societe francaise de rhumatologie. Published by Elsevier Masson SAS. All rights reserved. |
DOI | 10.1016/j.jbspin.2020.09.001 |