Osmotic Extraction of Hypotonic Fluid from the Lungs

Effros, Richard M.

doi:10.1172/jci107834

Cited by 54 publications

(19 citation statements)

References 28 publications

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“…The smaller the molecular size of the osmotic agent, the more hypotonic is the volume flux because it is localized more exclusively to the transcellular pathway. This prediction is in agreement with the observations of Effros (16). Our model predicts that about two-thirds of the fluid loss during a small-solute transient in the heart originates in the parenchymal cells.…”

Section: Errors and Limitationssupporting

confidence: 92%

“…In a whole organ, the total fluid movement across the capillary wall, J v S, is nearly equal to the rate of weight change of the organ; knowledge of the magnitude of ⌬⌸ and L p is all that is needed to estimate . Estimates of using this analysis method and osmotic weight transient measurements have been obtained in many mammalian tissues including heart (19,47,49,50), skeletal muscle (15,39), and lung (16,37). For small solutes like sucrose, estimates of in skeletal muscle range from 0.08 (39) to 0.41 (54) and in heart are 0.30 (49) and 0.14 (19).…”

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confidence: 99%

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Transient transcapillary exchange of water driven by osmotic forces in the heart

Kellen

Bassingthwaighte

2003

American Journal of Physiology-Heart and Circulatory Physiology

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Kellen, Michael R., and James B. Bassingthwaighte. Transient transcapillary exchange of water driven by osmotic forces in the heart. Am J Physiol Heart Circ Physiol 285: H1317-H1331, 2003. First published May 8, 2003 10.1152/ ajpheart.00587.2002.-Osmotic transient responses in organ weight after 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 with NaCl, urea, glucose, sucrose, raffinose, inulin, and albumin and analyzed the data with a new anatomically and physicochemically based model accounting 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 ϳ28% of the transcapillary water flux going to form lymph was through the endothelial cell membranes [capillary hydraulic conductivity (Lp) ϭ 1.8 Ϯ 0.6 ϫ 10 Ϫ8 cm ⅐ s Ϫ1 ⅐ mmHg Ϫ1 ], presumably mainly through aquaporin channels. The interendothelial clefts (with Lp ϭ 4.4 Ϯ 1.3 ϫ 10 Ϫ8 cm ⅐ s Ϫ1 ⅐ mmHg Ϫ1 ) account for 67% of the water flux; clefts are so wide (equivalent pore radius was 7 Ϯ 0.2 nm, covering ϳ0.02% 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 because 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 milliosmolar osmolarity change were 200 times larger than steady-state water flux. The analysis completely reconciles data from osmotic transient, tracer dilution, and lymph sampling techniques. capillary permeability; reflection coefficient; transport modeling; microcirculation; isolated rabbit heart; porous transport THE OSMOTIC WEIGHT TRANSIENT method is one of the few techniques available to measure the reflection coefficient ( ) of small hydrophilic solutes in the vascular beds of whole organs. Using a single-membrane model of events during this experiment, Vargas and Johnson (49) developed a relationship, ϭ J v /(L p S⌬⌸), where L p is capillary hydraulic conductivity, S is surface area, and ⌬⌸ is osmotic perturbation, which relates the volume flux across the capillary wall, J v , to the solute reflection coefficient, , immediately following a step change in perfusate osmolarity. In a whole organ, the total fluid movement across the capillary wall, J v S, is nearly equal to the rate of weight change of the organ; knowledge of the magnitude of ⌬⌸ and L p is all that is needed to estimate . Estimates of using this analysis method and osmotic weight transient measu...

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Section: Errors and Limitationssupporting

confidence: 92%

mentioning

confidence: 99%

Transient transcapillary exchange of water driven by osmotic forces in the heart

Kellen

Bassingthwaighte

2003

American Journal of Physiology-Heart and Circulatory Physiology

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“…Although electrolytes and sugars equilibrate with lung interstitial fluid within several minutes, 67 Taylor and Gaar 69 and Effros 70 have shown that it is possible to extract some water from the lung in the first several seconds following sudden sustained increases or single bolus injections of osmotically active crystalloid agents in isolated, perfused lungs.…”

Section: Crystalloidsmentioning

confidence: 99%

“…70 Since the endothelial cells, forming the lining of the microvascular bed in the lung, represent approximately 30% of the total extravascular tissue mass, 71 it is likely that a substantial fraction of the extracted water came from within the endothelial cells themselves; that is, the endothelial cells were dehydrated.…”

Section: Crystalloidsmentioning

confidence: 99%

Pulmonary edema due to increased microvascular permeability to fluid and protein.

Staub¹

1978

Circulation Research

175

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THE USUAL clinical designation of pulmonary edema as either cardiogenic or noncardiogenic implies a pathophysiology that is not necessarily true and, in the case of noncardiogenic edema, is singularly uninformative. A better classification would be one based upon the two major variables in the equation for transvascular fluid flow (Starling's equation), namely, Net fluid flow = conductance x driving pressure or, in symbols,where Qf is the net transvascular fluid flow, K is the fluid filtration coefficient, P is the hydrostatic pressure in the microvascular* lumen (mv) and perimicrovascular* interstitial fluid (pmv), respectively; a is a weighted plasma protein reflection coefficient which determines the "effective" transvascular protein osmotic pressure difference; and II is the protein osmotic pressure in the plasma (mv) and perimicrovascular (pmv) compartments, respectively.According to Equation 1, the two major types of edema are that due to increased driving pressure (high pressure edema) and that due to altered integrity of the microvascular membrane (permeability edema).High pressure edema may be of cardiac origin (increased microvascular hydrostatic pressure due to left atrial hypertension), but it also may occur when cardiac function is normal as in overexpansion of extracellular volume by crystalloid fluid infusions' (increased pulmo-

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“…The evidence supporting a distinct pathway for water flux is clear; Effros (22) demonstrated that the fluid extracted from lung tissues during an increase in perfusate osmolarity was essentially solute free, implying the existence of an additional, presumably transcellular, pathway across the capillary. The recent identification of the ubiquitous expression of aquaporin water channels in the endothelial cells of most organs (66) and the demonstration that the movement of osmotically driven water exchange can be inhibited by known inhibitors of aquaporins (16,23) have precisely identified the molecular basis for solute-free water movements.…”

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confidence: 99%

An integrative model of coupled water and solute exchange in the heart

Kellen

Bassingthwaighte

2003

American Journal of Physiology-Heart and Circulatory Physiology

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.-Physiologists have devised many models for interpreting water and solute exchange data in whole organs, but the models have typically neglected key aspects of the underlying physiology to present the simplest possible model for a given experimental situation. We have developed a physiologically realistic model of microcirculatory water and solute exchange and applied it to diverse observations of water and solute exchange in the heart. Model simulations are consistent with the results of osmotic weight transient, tracer indicator dilution, and steady-state lymph sampling experiments. The key model features that permit this unification are the use of an axially distributed blood-tissue exchange region, inclusion of a lymphatic drain in the interstitium, and the independent computation of transcapillary solute and solvent fluxes through three different pathways. microcirculation; capillary permeability; osmotic transient; lymph; multiple-indicator dilution PHYSIOLOGISTS ARE INTERESTED in the exchange of material between capillaries and their surrounding tissues because this process is fundamental to the viability of multicellular life. The kinetics of coupled solute-solvent exchange across capillary walls can be described phenomenologically by three parameters: the hydraulic conductivity (L p ), the permeability (P), and the reflection coefficient () (37). The values of these parameters can be determined by several experimental methods, including measurement of the outflow concentration time courses of solutes after a bolus injection of tracers (the multiple-tracer indicator dilution technique), gravimetric or isogravimetric measurements of the response to perturbations of osmotic or hydrostatic pressures (the osmotic transient method), and simultaneous measurements of solute concentrations in lymph and plasma (lymph sampling techniques). Reasonable fits to data from these sources have been obtained with relatively simple analytical methods, like the Crone-Renkin (18, 52) estimate of capillary permeability, the Vargas and Johnson (65) estimate of reflection coefficient, and the "pore-stripping" analysis of Renkin et al. (52a). These analysis methods have enjoyed widespread use in determining transport parameter values from indicator dilution, osmotic transient, and lymph data, respectively.Although mathematically independent, all three phenomenological transport parameters must ultimately arise from the physical and chemical properties of the exchanging solution and the anatomic structures that create the pathways for its exchange across capillary walls. Consequently, hydrodynamic models of solute and fluid movements through the endothelial cell junction, represented as idealized pores in the capillary wall, have been developed to relate the transport parameters to mechanistic quantities such as solute size and diffusion coefficient and pore radius and relative area (12,19,44,48,49). Even though there is no strict correspondence between the idealized pores and actual capillary morphology, pore models have proven...

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Osmotic Extraction of Hypotonic Fluid from the Lungs

Cited by 54 publications

References 28 publications

Transient transcapillary exchange of water driven by osmotic forces in the heart

Transient transcapillary exchange of water driven by osmotic forces in the heart

Pulmonary edema due to increased microvascular permeability to fluid and protein.

An integrative model of coupled water and solute exchange in the heart

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