Adjuvant-induced arthritis is a relevant model to mimic coronary and myocardial impairments in rheumatoid arthritis
| Autor: | Perle Totoson, Romain Bordy, Johnny Moretto, Karena Moretto-Riedweg, Sylvie Devaux, Céline Demougeot, Daniel Wendling |
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| Rok vydání: | 2020 |
| Předmět: |
Cardiac function curve
medicine.medical_specialty Ischemia Myocardial Ischemia Arthritis Arthritis Rheumatoid Rheumatology Internal medicine medicine Animals Humans Endothelial dysfunction biology business.industry Heart medicine.disease Angiotensin II Arthritis Experimental Pathophysiology Rats Rheumatoid arthritis cardiovascular system Cardiology biology.protein Creatine kinase business |
| Zdroj: | Joint bone spine. 88(1) |
| ISSN: | 1778-7254 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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