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The pathogenesis of degenerative joint disease (osteoarthritis) has been the subject of debate and conjecture for many years. Because the syndrome is found so often in older subjects, it would seem logical to correlate the general arteriosclerotic vascular changes with the degenerative joint pathology. However, the weight of investigative evidence has been against such a relationship, and the factors of "wear and tear" and "stress and strain" are considered to be the major forces in the development of degenerative joint diseases (1). In many instances where pathological changes of degenerative joint disease have been discovered, no complaint of pain or disability had been made (2, 3). It would appear that arteriosclerotic changes per se cannot explain degenerative joint disease (4, 5), and that vasomotor changes may play a significant role. In peripheral vascular disease, intra-arterial Priscoline® was reported to produce increased blood flow and to relieve pain and disability. It was therefore reasonable to expect a comparable effect in and around a joint and such an investigation was made by one of us (S.D.) in a series of patients with degenerative joint disease of the knee (6). Priscoline® (2benzylimidazoline hydrochloride), an adrenolytic and sympatholytic agent with a direct action upon autonomic nerve endings, was given by the intraarterial (femoral artery) route. In view of the beneficial subjective effect, a study was then made of intra-articular temperature changes in normal knee joints (7). This investigation demonstrated that the joint temperatures increased in normal subjects following intra-arterial sympatholytic agents (Priscoline®), presumably as a result of intra-articular vasodilatation. In another series of studies by one of us, the clearance rates of radioactive sodium from skin and muscle were investi-

THE CLEARANCE OF NA24 FROM THE NORMAL AND OSTEO-ARTHRITIC KNEE JOINT AND THE RESPONSE TO INTRA-ARTERIAL PRISCOLINE®1