Blake D R, Merry P, Unsworth J, Kidd B L, Outhwaite J M, Ballard R, Morris C J, Gray L, Lunec J
Inflammation Group, London Hospital Medical College.
Lancet. 1989 Feb 11;1(8633):289-93. doi: 10.1016/s0140-6736(89)91305-6.
A series of experiments showed that, on exercise of the inflamed human knee, intra-articular pressure rises above synovial capillary perfusion pressure, causing intra-articular hypoxia; and that, on cessation of exercise, there is oxidative damage to lipids and IgG within the joint. These findings are consistent with the hypothesis that persistence of synovial inflammation can be due to exercise-induced hypoxic-reperfusion injury mediated by reactive oxygen species.
一系列实验表明,在发炎的人膝关节运动时,关节内压力会升高至超过滑膜毛细血管灌注压,从而导致关节内缺氧;而在运动停止时,关节内的脂质和免疫球蛋白G会发生氧化损伤。这些发现与以下假设一致,即滑膜炎症的持续可能是由于活性氧介导的运动诱导的缺氧再灌注损伤所致。