Inulin Flux Research Articles

Pump and leak in regulation of fluid transport in rabbit cornea.

Rabbit corneas were isolated, denuded of epithelium, and perfused on the anterior and posterior surfaces with Krebs Ringer-bicarbonate with additions of 50 microM H2O2, 125 microM BCNU, or 100 microM ouabain. The permeability of the corneal endothelium to labelled mannitol and inulin was determined by adding these compounds to the endothelial perfusate and measuring the rate of appearance of radioactivity in the anterior perfusate. Both H2O2 and BCNU increased the flux of mannitol and inulin across the endothelium in a time dependent manner, but ouabain had no effect. Additions of glucose with H2O2 or of GSH with BCNU prevented the observed changes in permeability. ATPase activities in the endothelia of intact, isolated corneas were also determined following incubation in the same media. The only observable effects of H2O2 and BCNU were slight reductions in the activity of Na+ + K+ ATPase. It is concluded that permeability changes, the leak, are more critical than active transport processes, the pump, in determining the rate and extent of swelling that results from exposure of the cornea to these agents.

Non-electrolyte diffusion across the frog gastric mucosa under osmotic gradients

Serosal-to-mucosal and mucosal-to-serosal diffusion of 14C-labelled inulin, sucrose, erythritol and propionamide was compared with 3HHO diffusion in mucosae incubated with isosmotic solutions at both surfaces, as well as isosmotic solution at serosal surface and hyperosmotic solution at the mucosal surface. The use of a hyperosmotic solution at the mucosal surface significantly increases unidirectional diffusion fluxes of inulin and of sucrose. To a nonsignificant extent, it affects the fluxes of erythritol and propionamide and significantly reduces the 3HHO diffusion. A size increment of the diffusion path utilized by the larger molecules is proposed.

Distribution of three hexose derivatives across the pancreatic epithelium: Paracellular shunts or cellular passage?

It has been proposed that the pancreatic epithelium is permeable to three presumably passively distributed non-electrolytes, namely sucrose, inulin and mannitol, via paracellular shunts, and that the increased flux of sucrose and inulin seen during augmented digestive enzyme secretion is due to an increase in the permeability of these shunts. The present study considers this hypothesis by comparing the permeability of the epithelium to three different hexose derivatives, mannitol, inositol and 3- O-methyl-glucose, in both the unstimulated state and after the augmentation of protein secretion with a cholinergic drug. The epithelium was found to be more permeable to mannitol than to either inositol or 3- O-methyl-glucose. In the unstimulated state, the concentration of mannitol in ductal fluid at the steady state was approx. 54% of its concentration in the interstitium, as compared to 12% for inositol and 8% for 3- O-methyl-glucose. Cholinergic stimulation substantially increased the concentration of inositol and 3- O-methyl-glucose in secretion, but did not increase that of mannitol. The increase in the concentration of inositol occurred in the absence of an increase in its rate of transepithelial movement. Taken together, the results suggest that: (1) there is a substantial passage of mannitol through the cells of the epithelial layer, and (2) the increased concentration of inositol and 3- O-methyl-glucose in ductal fluid that occurs with stimulation is due to an increase in their efflux from secretory cells.

Rabbit corneal endothelial permeability in the presence and absence of adenosine and glutathione.

Rabbit corneal endothelial fluxes of sodium, bicarbonate, inulin, and dextran have been measured in ambient solutions containing either 0.5 mM adenosine alone (A), 0.3 mM glutathione alone (G), both adenosine and glutathione, or neither adenosine nor glutathione. Addition of A alone to a solution lacking both additives caused a decrease in both Jstrendo and Jendostr sodium fluxes coupled with an increase in Jstrendo net. Addition of G alone caused no effect, whereas addition of A and G together caused a decrease in both Jstrendo and Jendostr sodium fluxes and a large increase in Jstrendo net. Addition of A or G caused an increase in Jstrendo bicarbonate flux, but no change in Jendostr flux. Addition of A and G caused an increase in both Jstrendo and Jendostr bicarbonate flux and a decrease in Jstrendo net. None of the solution variations caused an alteration in either inulin or dextran permeability. Since both A and G influence Jstrendo net bicarbonate and sodium transport, this may provide an explanation of the beneficial effects of these compounds on the endothelium to both enhance and prolong corneal thickness and hydration regulation.

Solvent drag of large solutes indicates paracellular water flow in leaky epithelia

Net fluxes ( J s n ) of sucrose, inulin, dextran (relative molecular mass 15000–17000), albumin and haemoglobin were measured across guineapig gall bladder unilateral preparations in which the absorptive flow ( J v ) was varied over a wide range (without transepithelial osmotic gradients) by perfusing their lumina either with isosmotic solutions or with solutions of reduced osmolalities (a procedure that increased J v ). The absorptive flow J v was inhibited by 10 –4 M ouabain. The net flux J s n was a linear function of J v for sucrose, inulin and dextran, the slopes being inversely related to the size of the solute. Albumin and haemoglobin barely crossed the preparation. The large increase in J s n cannot be accounted for by increased leakiness of the preparation or by unstirred layer effects. The logarithms of the unidirectional flux ratios for sucrose, inulin and dextran in bilateral preparation were also linear functions of J v . It is concluded that solvent drags these solutes via the paracellular pathway. More than 50% of the water flows paracellularly also under normal physiological conditions, since J s n for sucrose was also a linear function of J v in experiments performed only at the physiological osmolality (0.3osm). This value is calculated from the slope of the line relating J s n to J v .

The mechanism of decreased intestinal sodium and water absorption after acute volume expansion in the rat.

Studies were performed in rat small intestine in vivo to determine the effect of saline infusion on intestinal transport of Na(+) and H(2)O. Saline infusion decreased net Na(+) flux (J(n) (Na)) from 12.7 +/-0.8 to 6.4 +/-1.5 muEq/hr per cm in the jejunum when the intestinal perfusate contained both Na(+) and glucose. A similar fall in J(n) (Na) occurred in ileum. When mannitol was substituted for glucose in the perfusate, control absorption decreased 29% in jejunum and 18% in ileum, but saline infusion still caused a decrease in J(n) (Na) quantitatively similar to that seen when glucose was present. When choline was substituted for Na(+) in the perfusate, there was net movement of Na(+) from blood to lumen during control and this net secretion was increased further after saline infusion. These observations suggest that saline infusion has a similar effect to decrease intestinal J(n) (Na) under three widely different conditions of basal sodium transport. Permeability of intestinal mucosa to inulin was very low under basal conditions but increased fivefold after saline infusion, and the unidirectional flux of Na(+) from blood to lumen doubled. This increase in unidirectional flux of Na(+) was greater than the observed decrease in J(n) (Na).Thus, saline infusion decreased net absorption of Na(+) and H(2)O from small intestine through mechanisms which did not appear to be dependent upon the rate of Na(+) flux from lumen to blood, and in association with an increased flux of inulin and Na(+) into the intestinal lumen. The data suggest that the effect of saline infusion to decrease net absorption from the intestine could be due either to an increase in passive permeability of the epithelium which could disrupt solute gradients within the membrane or to an increase in flow of solution into the intestinal lumen.