Levick J R, McDonald J N
Department of Physiology, St. George's Hospital Medical School, London, United Kingdom.
Microvasc Res. 1994 Jan;47(1):68-89. doi: 10.1006/mvre.1994.1006.
Fluid exchange in synovial joints involves both interstitial and transcapillary flow. Here the influence of intraarticular albumin, a normal component of intraarticular fluid, on net transsynovial flow was explored by infusing albumin solutions into the synovial cavity of rabbit knees and recording net flow across the synovial lining. The latter is a discontinuous cell layer possessing matrix-filled intercellular spaces and fenestrated capillaries. Albumin solutions (10-250 g.liter-1) of known oncotic pressure and viscosity were infused at a constant pressure between 3 and 18 cm H2O, either in vivo or post mortem. The rate of absorption (outflow) of Krebs solution from the cavity at the same pressure was measured as the control. Albumin reduced the net rate of absorption of fluid from the joint cavity (Qs). The reduction in Qs in vivo, expressed as a fraction of control, was greater than the fractional reduction in the fluidity of the albumin solution (i.e., 1/relative viscosity). At high albumin concentrations in vivo, the net flow reversed direction and became a net filtration into the joint cavity. The change in Qs per unit change in intraarticular oncotic pressure was then 29.7 x 10(-3) microliters.min-1.cm H2O-1. Even when there was continuous net outflow across the lining, however, as at lower albumin concentrations or higher joint pressures, the intraarticular albumin became diluted compared with the infusate. When synovial blood flow was stopped by killing the animal, albumin had less effect on net transsynovial outflow than that in vivo. Outflow was still reduced by albumin but the fractional reduction was now less than the fractional reduction in bulk fluidity. Also, intraarticular dilution was less marked postmortem than in vivo. The observations were compatible with the view that the net transsynovial flow in vivo comprised two opposing flows, namely, capillary (fenestral) filtration into the joint cavity and interstitial flow from cavity to subsynovium. These two flows were affected oppositely by albumin: filtration was enhanced by the oncotic pressure of albumin in the pericapillary interstitium, whereas interstitial flow was reduced by the effect of albumin on fluidity. The results also raised the issues of whether fenestral filtration reduces nearby interstitial albumin concentration and how interstitial and bulk-phase fluidities are related.
滑膜关节中的液体交换涉及组织间液流动和跨毛细血管流动。在此，通过将白蛋白溶液注入兔膝关节滑膜腔并记录滑膜衬里的净流量，探讨了关节内白蛋白（关节内液体的正常成分）对滑膜净流量的影响。滑膜衬里是一层不连续的细胞层，具有充满基质的细胞间隙和有窗孔的毛细血管。已知渗透压和粘度的白蛋白溶液（10 - 250 g·L⁻¹）在3至18 cm H₂O的恒定压力下进行体内或死后注入。在相同压力下，测量克雷布斯溶液从腔内的吸收（流出）速率作为对照。白蛋白降低了关节腔液体的净吸收速率（Qs）。体内Qs的降低，以对照的分数表示，大于白蛋白溶液流动性降低的分数（即1/相对粘度）。在体内高白蛋白浓度时，净流量方向逆转，变为向关节腔内的净滤过。然后关节内渗透压每单位变化时Qs的变化为29.7×10⁻³微升·分钟⁻¹·cm H₂O⁻¹。然而，即使在滑膜衬里存在持续的净流出时，如在较低白蛋白浓度或较高关节压力下，与注入液相比，关节内白蛋白仍被稀释。当通过处死动物使滑膜血流停止时，白蛋白对滑膜净流出的影响比在体内时小。白蛋白仍使流出减少，但现在降低的分数小于总体流动性降低的分数。此外，死后关节内稀释不如体内明显。这些观察结果与以下观点一致：体内滑膜净流量包括两个相反的流动，即毛细血管（窗孔）向关节腔内的滤过和从腔到滑膜下组织的组织间液流动。白蛋白对这两种流动的影响相反：毛细血管周围组织间隙中白蛋白的渗透压增强了滤过，而白蛋白对流动性的影响降低了组织间液流动。结果还提出了窗孔滤过是否会降低附近组织间白蛋白浓度以及组织间液和总体相流动性如何相关的问题。
