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Received April 25, 2002
Accepted after revision July 11, 2002
1 Division of Biomedical Sciences, Faculty of Medicine, Imperial College of Science Technology and Medicine, Exhibition Road, London SW7 2AZ and Medical Biophysics Group, School of Physics, University of Exeter, Exeter EX4 4XL, UK
2 Medical Biophysics Group, School of Physics, University of Exeter, Exeter EX4 4XL, UK
3 Sundial House, 24A High Street, Alderney, Guernsey GY9 3UG, UK
* To whom correspondence should be addressed. E-mail: c.c.michel{at}ic.ac.uk.
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)U x 10-5 + 0.44 (± 0.0291). Similarly, in nine rat venules, mean PS = 1.62 (± 0.385)U x 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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