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1 Department of Bioengineering, University of Washington, Seattle, WA, USA
* To whom correspondence should be addressed. E-mail: jbb{at}nsr.bioeng.washington.edu.
Osmotic transient responses in organ weight following changes in perfusate osmolarity have implied steric hindrance to small-molecule transcapillary exchange, but tracer methods do not. We obtained osmotic weight transient data in isolated Ringer-perfused rabbit hearts using NaCl, urea, glucose, sucrose, raffinose, inulin, and albumin, and analyzed the data with a new anatomically and physico-chemically based model which accounted for: (1) transendothelial water flux, (2) two sizes of porous passages across the capillary wall, (3) axial intracapillary concentration gradients, and (4) water fluxes between myocytes and interstitium. During steady-state conditions about 28% of the transcapillary water flux going to form lymph was through the endothelial cell membranes (Lp = [1.8 ± 0.6 x 10-8 cm s-1 mmHg-1), presumably mainly through aquaporin channels. The interendothelial clefts (with Lp = [4.4 ± 1.3] x 10-8 cm s-1 mmHg-1) account for 67% of the water flux; clefts are so wide (equivalent pore radius was 7 ± 0.2 nm, covering about 0.02% of the capillary surface area) that there is no apparent hindrance for molecules as large as raffinose. Infrequent large pores account for the remaining 5% of the flux. During osmotic transients due to 30 mM increases in concentrations of small solutes, the transendothelial water flux was in the opposite direction and almost 800 times as large, and was entirely transendothelial since no solute gradient forms across the pores. During albumin transients, gradients persisted for long times because albumin does not permeate small pores; the water fluxes per mM osmolarity change were 200 times larger. The analysis completely reconciles data from osmotic transient, tracer dilution, and lymph sampling techniques.
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