Objectives: Because fibroblast filamentous actin (F-actin) influences cutaneous interstitial matrix swelling pressure (5), we investigated whether F-actin in fibroblast-derived synoviocytes influences the hydraulic permeability of the transsynovial interstitial pathway. The study also tested whether F-actin in fenestrated synovial endothelium contributes to the blood-joint barrier in vivo. Methods: The clearance of Evans blue-albumin (EVA) from plasma into the knee joint cavity was determined in joint infused with F-actin disrupting cytochalasin D (1-200 M), latrunculin B (100 M) or vehicle in anesthetized rabbits. The hydraulic permeability of the lining was determined as the slope relating net trans-synovial flow Q s to intra-articular pressure P j . Synovium was examined histologically after i.v. Monastral blue to assess endothelial leakiness. Results: EVA permeation in vivo was increased up to 25-fold by cytochalasin (p ס 0.0002, ANOVA), with an EC 50 of 23 M (95% confidence limits 13-43 M). Washout quickly reversed the increase. Latrunculin had a similar effect. F-actin disruption switched Q s from drainage (control) to filtration into the cavity at low P j in vivo and raised the conductance dQ s /dP j by 2.13 (p ס 0.001, ANOVA). Circulatory arrest abolished these effects. Monastral blue revealed numerous endothelial leaks. Conclusions: F-actin is crucial to the barrier function of fenestrated endothelium in situ. No significant effect of synoviocyte F-actin on matrix permeability was detected.
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