PEPITE EA 4267, FHU INCREASE, University Bourgogne Franche-Comté, 25000 Besançon, France.
EA 4266 EPILAB, University Bourgogne Franche-Comté, 25000 Besançon, France; Service de Rhumatologie, CHU Minjoz, 25000 Besançon, France.
Joint Bone Spine. 2021 Jan;88(1):105069. doi: 10.1016/j.jbspin.2020.09.001. Epub 2020 Sep 10.
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.
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.
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.
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.
确定佐剂性关节炎模型是否再现了类风湿关节炎患者中观察到的冠状动脉和心脏损伤。研究了疾病活动与血管紧张素 II 和内皮素-1 的循环水平之间的联系，以及心肌对缺血的易感性。
在急性炎症期，评估了分离动脉中的冠状动脉反应性，并在整体缺血/再灌注前后研究了分离灌注心脏的心脏功能。通过冠状动脉流出物中的梗死面积、乳酸脱氢酶和肌酸磷酸激酶水平来评估缺血损伤。测量了心肌髓过氧化物酶活性以及血管紧张素 II 和内皮素-1 水平。
与对照组相比，佐剂性关节炎的乙酰胆碱诱导的冠状动脉舒张反应降低，与心脏肥大有关，两者均与血浆内皮素-1 和血管紧张素 II 以及关节炎评分相关。尽管基线时心脏功能相似，但佐剂性关节炎大鼠在缺血/再灌注后表现出较低的心脏功能恢复、较高的髓过氧化物酶活性、较大的梗死面积和肌酸磷酸激酶水平。
佐剂性关节炎模型显示出与心肌肥大相关的冠状动脉内皮功能障碍和对缺血的耐受性降低。该模型可能有助于解析类风湿关节炎中心脏功能障碍的病理生理学，并为研究内皮素-1 和血管紧张素 II 的作用铺平道路。
