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The permeability, PS, to sodium fluorescein (Stokes-Einstein radius = 0.45 nm) has been measured in single mesenteric capillaries of pithed frogs and anaesthetised rats as perfusion velocity, U, was varied over a range from 400 up to 2000-10 000 µm s-1. PS increased linearly with U. In 20 frog capillaries, mean (± S.E.M.) PS (in µm s-1) = 9.35 (± 1.55)U10-5 + 0.244 (± 0.0291). Similarly, in nine rat venules, mean PS = 1.62 (± 0.385)U
10-4 + 0.375 (± 0.025). The flow-dependent component of permeability could be reversibly abolished in frog capillaries by superfusing with 100 µM noradrenaline and by superfusing rat venules with the nitric oxide synthase inhibitor, NG-nitro-L-arginine (20 µM). It was shown that changes in microvascular pressure accompanying changes in U during free perfusion could account for only 15 % of the changes in PS, i.e. 85 % of the changes in PS were changes in the permeability coefficient itself. A comparison between the changes in PS with U and the previously described changes in microvascular permeability to K+ with U, suggest that if the flow-dependent component of permeability is modelled as a population of pores of constant size, these have radii of 0.8 nm. Such a pathway would limit flow-dependent permeability to small hydrophilic molecules and have minimal effect on net fluid exchange.
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