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

Kellen, Michael R.; Bassingthwaighte, James B.

doi:10.1152/ajpheart.00587.2002

Cited by 36 publications

(26 citation statements)

References 56 publications

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“…A similar value of capillary wall reflection coefficient for glucose, G cap ϭ 0.6, was assumed previously (54). The capillary wall reflection coefficients for glucose and urea, of G cap ϭ 0.28 and U cap ϭ 0.29, respectively, were found in the heart muscle (24). The experimental values were obtained using the osmotic transient technique in isolated organs that is based on transiently increased plasma osmolality of inlet blood and the decrease in small-solute concentrations in outlet blood that follows the inflow of water to the capillaries induced by the osmotic gradient between blood and interstitial fluid (24,57,59).…”

Section: Model Parameterssupporting

confidence: 78%

Computer simulations of osmotic ultrafiltration and small-solute transport in peritoneal dialysis: a spatially distributed approach

Stachowska-Piętka

Waniewski

Flessner

et al. 2012

American Journal of Physiology-Renal Physiology

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The aim of this study was to simulate clinically observed intraperitoneal kinetics of dialysis fluid volume and solute concentrations during peritoneal dialysis. We were also interested in analyzing relationships between processes in the peritoneal cavity and processes occurring in the peritoneal tissue and microcirculation. A spatially distributed model was formulated for the combined description of volume and solute mass balances in the peritoneal cavity and flows across the interstitium and the capillary wall. Tissue local parameters were assumed dependent on the interstitial hydration and vasodilatation induced by glucose. The model was fitted to the average volume and solute concentration profiles from dwell studies in 40 clinically stable patients on chronic ambulatory peritoneal dialysis using a 3.86% glucose dialysis solution. The model was able to describe the clinical data with high accuracy. An increase in the local interstitial pressure and tissue hydration within the distance of 2.5 mm from the peritoneal surface of the tissue was observed. The penetration of glucose into the tissue and removal of urea, creatinine, and sodium from the tissue were restricted to a layer located within 2 mm from the peritoneal surface. The initial decline of sodium concentration (sodium dip) was observed not only in intraperitoneal fluid but also in the tissue. The distributed model can provide a precise description of the relationship between changes in the peritoneal tissue and intraperitoneal dialysate volume and solute concentration kinetics. Computer simulations suggest that only a thin layer of the tissue within 2–3 mm from the peritoneal surface participates in the exchange of fluid and small solutes between the intraperitoneal dialysate and blood.

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Section: Model Parameterssupporting

confidence: 78%

Computer simulations of osmotic ultrafiltration and small-solute transport in peritoneal dialysis: a spatially distributed approach

Stachowska-Piętka

Waniewski

Flessner

et al. 2012

American Journal of Physiology-Renal Physiology

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show abstract

“…Normal junctions are impermeable for LDL, so the reflection coefficient r nj ¼ 1. Expression for the overall reflection coefficient of the endothelium can be calculated from r for each of the individual pathways from heteroporous model [42][43][44]. Similarly to (13) we have:…”

Section: Wss Dependent Mechanism Of the Ldl Transport By The Endotheliummentioning

confidence: 99%

Effects of shear stress on low-density lipoproteins (LDL) transport in the multi-layered arteries

Jesionek

Kostur

2015

International Journal of Heat and Mass Transfer

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“…Myocardial edema is associated with a significant reduction in cardiac performance in ischemia/reperfusion and cardiopulmonary bypass. In a number of clinically significant situations, including those mentioned, the endothelial AQP-l has been proposed to be primarily responsible for the movement of water out of the interstitial space and into the capillaries (14). The involvement of the AQPs in the development of tissue edema has been also demonstrated in several noncardiac tissues, such as the brain, and avascular tissues, such as the cornea (15).…”

mentioning

confidence: 99%

Attenuated Expression and Gelsolin in Association with Induction of Aquaporin-1 and Nitric Oxide Synthase in Dysfunctional Hearts of Aging Mice Exposed to Endotoxin

Madonna

Jiang

Geng

2012

Int J Immunopathol Pharmacol

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Sepsis triggered by endotoxinemia may impair cardiac function. A decline in tolerance to septic shock occurs with aging. This study addressed the hypothesis that aging negatively impairs expression of gelsolin, and axerts the regulatory effects on the water channel protein aquaporin-l (AQP-l) and endotoxin-inducible nitric oxide synthase (iNOS). We explored whether the age-related gene changes are associated with the cardiac dysfunction induced by endotoxic stress exposure. Male mice at young (-3-month) and old (-12-month) ages received intraperitoneal injections of saline or lipopolysaccharide (LPS, 30mg/Kg). Cardiac performance and morphology were analyzed by echocardiography at baseline and 2 and 24 hafter injection. At the end of treatment, the animals were sacrificed, and cardiac tissues were collected for assessing expression of gelsolin, AQP-l, iNOS, and transcription-3 (STAT3). LPS administration led to a decreased contractility while increasing cardiac dimensions in both young and old mice. LPS also markedly induced expression of gelsolin in both animal groups. However, compared to young mice, old mice showed compromised induction of gelsolin and cardiac performance in response to endotoxin. Meanwhile, the LPS-exposed old animals exhibited higher levels of AQP-l, iNOS, and phosphorylated STAT3. Gelsolin-null mice had increased expression of glycosylated AQP-l and STAT3 phosphorylation as well as cardiac dysfunction. Thus, endotoxin administration induces expression of gelsolin, AQP-l and pro-inflammatory genes, such as iNOS. Our data suggest that changed expression of gelsolin, AQP-l and iNOS may contribute to dysfunction of hearts in aged subjects with septic endotoxinemia.Sepsis ischaracterizedby multi-organ dysfunction, including cardiovascular dysfunction. Although the precise mechanism of the myocardial dysfunction that occurs during endotoxic stress exposure is not well defined, increasing experimental evidence suggests that the main molecular mechanisms include activation of various cytokines and inflammatory factors, increased vascular permeability, cytoskeleton remodeling, and induction of nitric oxide synthase (iNOS) with the subsequent generation of nitric oxide (NO). Sepsis predominantly affects older persons, and yet experimental data exploring septic

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

Cited by 36 publications

References 56 publications

Computer simulations of osmotic ultrafiltration and small-solute transport in peritoneal dialysis: a spatially distributed approach

Computer simulations of osmotic ultrafiltration and small-solute transport in peritoneal dialysis: a spatially distributed approach

Effects of shear stress on low-density lipoproteins (LDL) transport in the multi-layered arteries

Attenuated Expression and Gelsolin in Association with Induction of Aquaporin-1 and Nitric Oxide Synthase in Dysfunctional Hearts of Aging Mice Exposed to Endotoxin

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