Objective: To provide quantitative assessment of forces affecting filtration of synovial fluid in response to incremental changes in arterial and venous hemodynamics.
Animals: 7 clinically normal adult horses.
Procedure: Using a stationary, isolated metacarpophalangeal joint preparation, blood flow (Qa[cir]), tissue perfusion, arterial pressure (Pa[cir]), venous pressure (Pv[cir]), transsynovial fluid flow, total vascular resistance, vascular compliance, and tissue compliance were evaluated before and after arterial and venous pressure manipulations. At isogravimetric conditions, pre- and postcapillary resistance and ratios, osmotic reflection coefficient (sigma[d]), capillary pressure, net filtration pressure, and transitional microvascular pressure were determined.
Results: Synovial tissue blood flow was similar before, immediately after, and 3.5 hours after joint isolation. The sigma(d) for the joint was low, owing to the high oncotic pressure of synovial fluid at filtration-independent states. Transsynovial flow occurred in preference to lymph flow because of the high permeability of synovial tissue (low sigma[d]). Synovial fluid production and transfluid flow (synovium weight gain) increased at Pa(cir) > 200 mm of Hg, indicating a threshold phenomenon for synovial filtration. Net filtration pressure > 6 mm of Hg is needed to effect an increase in synovial fluid flow, and pressure of approximately 11 mm of Hg is necessary to increase lymphatic flow. Vascular compliance in the joint was low, but increased markedly with Pv(cir). Vascular and tissue compliance increased with increased Pa(cir). Vascular compliance changes caused by increased arterial pressure were minimal, compared with those caused by increased venous pressure owing to the greater elastance of arteries and the larger muscular arterial wall.
Conclusion: This isolated joint preparation permitted evaluation of codependent hemodynamic, microvascular, and transsynovial flow responses to hemodynamic manipulations. Synovial tissue permeability was markedly affected by increased vascular forces altering filtration pressures toward synovial fluid production.