Effects of electric charge on osmotic flow across periodically arranged circular cylinders

An electrostatic model is developed for osmotic flow across a layer consisting of identical circular cylinders with a fixed surface charge, aligned parallel to each other so as to form an ordered hexagonal arrangement. The expression of the osmotic reflection coefficient is derived for spherical solutes with a fixed surface charge suspended in an electrolyte, based on low-Reynolds-number hydrodynamics and a continuum, point-charge description of the electric double layers. The repulsive electrostatic interaction between the surface charges with the same sign on the solute and the cylinders is shown to increase the exclusion region of solute from the cylinder surface, which enhances the osmotic flow. Applying the present model to the study of osmotic flow across the endothelial surface glycocalyx of capillary walls has revealed that this electrostatic model could account well for the reflection coefficients measured for charged macromolecules, such as albumin, in the physiological range of charge density and ion concentration.

Protective effects of intravascular pressure and nitric oxide in ischemic lung injury

Cessation of blood flow during ischemia will decrease both distending and shear forces exerted on endothelium and may worsen ischemic lung injury by decreasing production of nitric oxide (NO), which influences vascular barrier function. We hypothesized that increased intravascular pressure (Piv) during ventilated ischemia might maintain NO production by increasing endothelial stretch or shear forces, thereby attenuating ischemic lung injury. Injury was assessed by measuring the filtration coefficient ( Kf) and the osmotic reflection coefficient for albumin (ςalb) after 3 h of ventilated (95% O2-5% CO2; expiratory pressure 3 mmHg) ischemia. Lungs were flushed with physiological salt solution, and then Piv was adjusted to achieve High Piv (mean 6.7 ± 0.4 mmHg, n = 15) or Low Piv (mean 0.83 ± 0.4 mmHg, n = 10). NG-nitro-l-arginine methyl ester (l-NAME; 10−5M, n = 10), NG-nitro-d-arginine methyl ester (d-NAME; 10−5M, n = 11), orl-NAME (10−5M)+l-arginine (5 × 10−4M, n = 6) was added at the start of ischemia in three additional groups of lungs with High Piv. High Piv attenuated ischemic injury compared with Low Piv (ςalb0.67 ± 0.04 vs. 0.35 ± 0.04, P < 0.05). The protective effect of High Piv was abolished byl-NAME (ςalb0.37 ± 0.04, P < 0.05) but not byd-NAME (ςalb0.63 ± 0.07). The effects of l-NAME were overcome by an excess of l-arginine (ςalb0.56 ± 0.05, P < 0.05). Kfdid not differ significantly among groups. These results suggest that Piv modulates ischemia-induced barrier dysfunction in the lung, and these effects may be mediated by NO.

Basic determinants of epicardial transudation

Myocardial edema formation, which has been shown to compromise cardiac function, and increased epicardial transudation (pericardial effusion) have been shown to occur after elevation of myocardial venous and lymphatic outflow pressures. The purposes of this study were to estimate the hydraulic conductance and osmotic reflection coefficient for the epicardium and to determine the effect of coronary sinus hypertension and cardiac lymphatic obstruction on epicardial fluid flux (JV,e/Ae). A Plexiglas hemispheric capsule was attached to the left ventricular epicardial surface of anesthetized dogs. JV,e/Ae was determined over 30-min periods for three intracapsular pressures (-5, -15, and -25 mmHg) and two intracapsular solutions exerting colloid osmotic pressures of 7.0 and 2.0 mmHg. Hydraulic conductance was estimated to be 3.7 +/- 0.5 microliters.h-1.cm-2.mmHg-1. An osmotic reflection coefficient of 0.9 was calculated from the difference in JV,e/Ae of 16.5 +/- 8.4 microliters.h-1.cm-2 between the two solutions. Graded coronary sinus hypertension induced a linear increase in JV,e/Ae, which was significantly greater in dogs without cardiac lymphatic occlusion than in those with occlusion.

Protein osmotic pressure gradients and microvascular reflection coefficients

Microvascular membranes are heteroporous, so the mean osmotic reflection coefficient for a microvascular membrane (sigma d) is a function of the reflection coefficient for each pore. Investigators have derived equations for sigma d based on the assumption that the protein osmotic pressure gradient across the membrane (delta II) does not vary from pore to pore. However, for most microvascular membranes, delta II probably does vary from pore to pore. In this study, we derived a new equation for sigma d. According to our equation, pore-to-pore differences in delta II increase the effect of small pores and decrease the effect of large pores on the overall membrane osmotic reflection coefficient. Thus sigma d for a heteroporous membrane may be much higher than previously derived equations indicate. Furthermore, pore-to-pore delta II differences increase the effect of plasma protein osmotic pressure to oppose microvascular fluid filtration.

Theoretical Analysis of Osmotic Agents in Peritoneal Dialysis. What Size is An Ideal Osmotic Agent?

In this article the difference between osmotic fluid flow (ultrafiltration) as driven by osmotic pressure and diffusion through thin leaky membranes is discussed. It is pointed out that water transport induced by osmosis is fundamentally different from the process of water diffusion. Applying modern hydrodynamic pore theory, the molar solute concentration and the solute concentration in grams per 100 mL, exerting the same initial transmembrane osmotic pressure as a 1% glucose solution, was investigated as a function of solute molecular weight (MW). It was then assumed, based on experimental data, that the major pathway responsible for the peritoneal osmotic barrier characteristics is represented by pores of radius ~47 å. With increasing solute radius, the osmotic reflection coefficient (σ) and, hence, the osmotic efficiency per mole of solute will increase. However, simultaneously, the molar concentration per unit solute weight will decrease. The balance point between these two events apparently occurs at a solute MW of approximately 1 kCa. An additional advantage of using solutes of high MW as osmotic agents during peritoneal dialysis (PC), rather than increased osmotic efficiency per se, lies in the fact that large solutes, due to their low peritoneal diffusion capacity, will maintain a sustained rate of ultrafiltration (osmosis) over a prolonged period. To illustrate this, we have performed computer simulations of peritoneal fluid transport according to the three-pore model of peritoneal permselectivity. According to these simulations, 4% of an 800 Ca polymer solution (+50 mmol/ L above isotonicity) will produce the same cumulative amount of intraperitoneal fluid volume ultrafiltered (UF) during 360 -400 minutes as 4% of a 2 kCa polymer solution (+20 mmol/L) or 6.5% of a 10 kCa polymer solution (+6.5 mmol/L) having the same electrolyte concentration as dialysis solutions conventionally used for PC. Similar cumulative UF volumes (during 400 minutes) can be obtained by a 2.5% glycerol (+272 mmol/L) or a 3.2% glucose-containing dialysis solution (+177 mmol/L) with conventional electrolyte composition.

Effects of oxygen tension and glucose concentration on ischemic injury in ventilated ferret lungs

In the ventilated ischemic lung, oxygen tension will increase at a time when glucose depletion may impair antioxidant defenses, thereby predisposing the lung to injury mediated by oxygen radicals. In the unventilated ischemic lung, however, glucose depletion in the setting of low oxygen tension may decrease production of ATP, leading to injury by a different mechanism. In this study, we evaluated the role of both oxygen tension and glucose concentration on ischemic injury in isolated ferret lungs. Injury, defined as an increase in vascular permeability, was assessed by measurement of filtration coefficient (Kf) and osmotic reflection coefficient for albumin (sigma alb) after 3 h of normothermic (37 degrees C) ischemia without reperfusion. Lungs were ventilated with either 95% O2–5% CO2 or 0% O2–5% CO2. The vasculature was flushed with physiological salt solution containing either 15 mM glucose (hyperoxia-glucose, anoxia-glucose), 15 mM sucrose (hyperoxia-sucrose, anoxia-sucrose), or no substrate (hyperoxia-no substrate, anoxia-no substrate) (n = 6 for each condition). Kf and sigma alb in hyperoxia-no substrate group did not differ from values in minimally ischemic normoxic normoglycemic ferret lungs. Without glucose, ischemic injury was worse in anoxic than in hyperoxic lungs. With glucose, ischemic injury was worse in hyperoxic than in anoxic lungs. Glucose exacerbated injury in hyperoxic, but not anoxic, lungs. These results indicate that ischemic injury in these lungs depended on both oxygen tension and glucose concentration and suggest that both oxygen radical generation and ATP depletion during ischemia may contribute to the development of this injury.

Separate effects of ischemia and reperfusion on vascular permeability in ventilated ferret lungs

In systemic organs, ischemia-reperfusion injury is thought to occur during reperfusion, when oxygen is reintroduced to hypoxic ischemic tissue. In contrast, the ventilated lung may be more susceptible to injury during ischemia, before reperfusion, because oxygen tension will be high during ischemia and decrease with reperfusion. To evaluate this possibility, we compared the effects of hyperoxic ischemia alone and hyperoxic ischemia with normoxic reperfusion on vascular permeability in isolated ferret lungs. Permeability was estimated by measurement of filtration coefficient (Kf) and osmotic reflection coefficient for albumin (sigma alb), using methods that did not require reperfusion to make these measurements. Kf and sigma alb in control lungs (n = 5), which were ventilated with 14% O2–5% CO2 after minimal (15 +/- 1 min) ischemia, averaged 0.033 +/- 0.004 g.min-1.mmHg-1.100 g-1 and 0.69 +/- 0.07, respectively. These values did not differ from those reported in normal in vivo lungs of other species. The effects of short (54 +/- 9 min, n = 10) and long (180 min, n = 7) ischemia were evaluated in lungs ventilated with 95% O2–5% CO2. Kf and sigma alb did not change after short ischemia (Kf = 0.051 +/- 0.006 g.min-1.mmHg-1.100 g-1, sigma alb = 0.69 +/- 0.07) but increased significantly after long ischemia (Kf = 0.233 +/- 0.049 g.min-1 x mmHg-1 x 100 g-1, sigma alb = 0.36 +/- 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of lymphatic protein flux data. V. Unique PS products and sigma dS at low lymph flows

The selectivity of the capillary membrane to protein (osmotic reflection coefficient, sigma d) can be measured at high transcapillary volume flow when the capillary membrane can be considered as a true sieve. However, the diffusive capacity of the membrane (permeability-surface area product, PS) for macromolecules has not been directly measured, only estimated by assuming that transcapillary volume flow was zero. Based on unique properties of the Peclet number, a parameter that describes the ratio of solute convective flux relative to diffusive capacity, we have developed three new techniques using lymph protein fluxes to estimate a unique PS product that is independent of transcapillary fluid flux. Two of these techniques require a measure of sigma d when the ratio of protein concentration in lymph relative to plasma is equal to (1- sigma d), which occurs at high capillary filtration rates. However, the third method allows both sigma d and the PS product to be determined at relatively low lymph flow rates, eliminating the need for high capillary pressures to determine sigma d. For each protein, these techniques yield an estimate of PS and sigma d for the total membrane. However, by analysis of several different sized proteins and estimation of small- and large-pore volume flows, sigma d and PS can be determined separately for the small- and large-pore pathways. These techniques for estimating sigma d and PS were evaluated by modeling the total solute flux of albumin and immunoglobulins G and M in a heteroporous membrane.