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A case of rupture of the flexor carpi radialis tendon in association with scapho-trapezial osteoarthritis is reported. The symptoms of pain and swelling contrast with the loss of function which characterizes rupture of other tendons in the hand and wrist.

SUMMARY It is postulated that the mobile inflamed joint may be subject to cyclical ischaemic reperfusion injury. Xanthine oxidoreductase is an enzyme thought to contribute to oxidative reperfusion injury, and the detection of this activity in human synovium is described. Three normal and five rheumatoid tissues were assayed with a carbon-14 radioassay detecting the conversion of [14C]xanthine to [14C]uric acid. Rheumatoid synovia contained 067-305 ,uU/g tissue (n=5), while normal synovia contained 1-2-5-0 ,uU/g tissue (n=3).Key words: reperfusion, ischaemia, ischaemic reperfusion, xanthine oxidase, xanthine, rheumatoid arthritis.We have previously suggested a mechanism involving ischaemic reperfusion injury to account for the unusual persistence of synovial inflammation.' This involved synovial ischaemia induced by exercise and reperfusion injury occurring on resting. In resting inflamed joints with an effusion, intra-articular pressures are raised compared with those of normal joints, but during exercise the pressure in these joints increases further.2 Lund-Olsen showed that partial pressures of oxygen (Po2) in the synovial fluid are lower in rheumatoid joints than in osteoarthritic or traumatised joints and fall during exercise.3 It is probable that, as the pressures measured during exercise often exceed the capillary perfusion pressure and indeed are greater than systolic blood pressure,24 occlusion of the vessels supplying the synovium occurs, explaining the drop in synovial fluid Po2. Once exercise has ceased intra-articular pressures drop and Po2 levels rise, often above basal levels, consistent, not only with reflow through the synovial vascular bed, but with a reactive hyperaemia.In many tissues much of the damage resulting from an ischaemic incident has been attributed to the postischaemic reperfusion phase,5 the ischaemic phase 'priming' the cells for the destructive activity occurring in the reperfusion phase. During temporary ischaemia low oxygen concentrations halt mitochondrial oxidative phosphorylation, and cellu-

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