Coderre Terence J, Wall Patrick D
Cerebral Functions Research Group, Department of Anatomy and Embryology, University College London, London WC1E 6BT U.K.
Pain. 1987 Mar;28(3):379-393. doi: 10.1016/0304-3959(87)90072-8.
Injection of sodium urate crystals into one ankle joint in the rat produces arthritis which is fully developed within 24 h. The time-course and dose-response of associated inflammation and sensory abnormalities are described. Following intra-articular sodium urate rats reduce the weight placed on the paw of the treated hind limb and develop a limp in their gait. The ankle swells and becomes more sensitive to pressure and passive movements. Touch, pressure and thermal stimuli applied to the foot distal to the treatment produce decreased responses, presumably because active flexion movements are noxious. Joint pathology is reflected by tissue oedema and the infiltration of polymorphonuclear leucocytes. However, there is no destruction or decrease in density of bone. It is proposed that this model of arthritis may have ethical and scientific advantages over adjuvant arthritis in the study of some aspects of the neural mechanisms of arthritis.
向大鼠的一个踝关节注射尿酸钠晶体可引发关节炎，该关节炎在24小时内完全形成。本文描述了相关炎症和感觉异常的时间进程及剂量反应。关节内注射尿酸钠后，大鼠会减少置于治疗后肢爪子上的重量，并出现跛行步态。踝关节肿胀，对压力和被动运动更加敏感。对治疗部位远端足部施加的触觉、压力和热刺激会导致反应降低，推测是因为主动屈曲运动会产生有害影响。关节病理表现为组织水肿和多形核白细胞浸润。然而，没有骨质破坏或骨密度降低的情况。有人提出，在研究关节炎神经机制的某些方面，这种关节炎模型可能比佐剂性关节炎具有伦理和科学优势。
