Blood-tissue transport of exogenous albumin and immunoglobulin G in genetically analbuminemic rats

Tracer uptake studies were carried out in adult female Nagase (NA) strain analbuminemic rats [derived from Sprague-Dawley (SD) stock] and in adult female SD controls to determine the extent to which capillary permeability to plasma proteins is altered in the absence of endogenous albumin. Accessory measurements (arterial pressure, central venous pressure, plasma and interstitial fluid protein concentrations and oncotic pressures, plasma volume, and interstitial fluid volume) confirm the report of Joles et al. [Am. J. Physiol. 257 (Renal Fluid Electrolyte Physiol. 26): F23-F28, 1989] that shows elevated plasma volumes, normal interstitial fluid volumes, nearly normal plasma oncotic pressures (due to elevated globulin concentrations), and lower interstitial fluid oncotic pressures. In skin, skeletal muscles, and heart muscle, clearances of exogenous heterologous (bovine) albumin were 20–40% higher in NA than in SD controls. In intestine, albumin clearances were 20–30% lower. In NA rats blood-to-tissue clearances of heterologous (bovine) immunoglobulin G in skin and heart were higher and in the intestine they were lower than in SD controls; however, clearances in skeletal muscles were not elevated. The differences between NA and SD are small compared with the large increases in macromolecular permeabilities reported by others for organs and single microvessels perfused with albumin-free fluids.(ABSTRACT TRUNCATED AT 250 WORDS)

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Microvascular exchange and interstitial volume regulation in the rat: implications of the model

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1989.257.6.h2081 ◽

1989 ◽

Vol 257 (6) ◽

pp. H2081-H2091 ◽

Cited By ~ 5

Author(s):

R. K. Reed ◽

B. D. Bowen ◽

J. L. Bert

Keyword(s):

Volume Regulation ◽

Interstitial Fluid ◽

Venous Pressure ◽

Flow Characteristics ◽

Experimental Information ◽

Fluid Volume ◽

Exchange System ◽

Interstitial Volume ◽

Interstitial Fluid Volume ◽

Fluid Volume Regulation

The present work uses and extends a dynamic mathematical model [J. L. Bert, B. D. Bowen, and R. K. Reed. Am. J. Physiol. 254 (Heart Circ. Physiol. 23): H384-H399, 1988] to investigate microvascular exchange and interstitial fluid volume regulation in the rat. Alternative concepts of transcapillary exchange as well as other parametric changes were incorporated into the model. In all cases, predictions resulting from these changes did not describe the available experimental information as well as the original model. A sensitivity analysis of the model showed the microvascular exchange system to be well regulated near its normal steady-state conditions through passive readjustment of the forces participating in the volume regulation. The transient rates of fluid and protein exchange were studied in order to determine the mechanisms inherent in the model that lead to fluid volume regulation during episodes of increased venous pressure and hypoproteinemia. In addition to interstitial compliance, lymph flow characteristics, and washdown of interstitial proteins, it was found that the magnitude and direction of reabsorption played an important role in the regulation process. Edema was always associated with a permanent reversal of the reabsorptive flow.

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A Lumped Parameter Mathematical Model of the Splanchnic Circulation

Journal of Biomechanical Engineering ◽

10.1115/1.2891375 ◽

1992 ◽

Vol 114 (2) ◽

pp. 222-226 ◽

Cited By ~ 3

Author(s):

Tai-Ming Chu ◽

Narender P. Reddy

Keyword(s):

Mathematical Model ◽

Interstitial Fluid ◽

Venous Pressure ◽

Splanchnic Circulation ◽

Governing Equations ◽

Liver Sinusoids ◽

Interstitial Fluid Volume ◽

Lumped Parameter ◽

Simulation Results ◽

Present Simulation

A lumped parameter mathematical model to describe the propulsion of blood in the splanchnic circulation was developed by integrating the principles of mechanics and physiology. A set of governing equations by derived by specifically considering the contractility of the portal vein, hepatic vein, liver sinusoids, and of the draining lymphatics. These equations were then simulated on a computer. The present simulation results substantiate previous experimental observations that hepatic venous pressure leads to portal hypertension and increased liver interstitial fluid volume.

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Exclusion phenomenon in the liver interstitium

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1982.243.5.g410 ◽

1982 ◽

Vol 243 (5) ◽

pp. G410-G414

Author(s):

J. A. Barrowman ◽

M. A. Perry ◽

P. R. Kvietys ◽

D. N. Granger

Keyword(s):

Interstitial Fluid ◽

Gamma Globulin ◽

Volume Fraction ◽

Venous Pressure ◽

Extracellular Volume ◽

Molecular Size ◽

Human Albumin ◽

Fourfold Increase ◽

Interstitial Volume ◽

Interstitial Fluid Volume

Measurements were made of hepatic interstitial fluid volume and the proportion of that space occupied by 125I-labeled lactoglobulin, albumin, and gamma-globulin in anesthetized cats. 51Cr-red blood cells and 99mTc-diethylenetriaminepentaacetic acid were used to estimate tissue blood volume and extracellular volume, respectively. Hepatic lymph was assumed to represent the interstitial fluid of the liver. The degree of exclusion of each protein increased with increasing molecular size. At normal hepatic venous pressures, the excluded volume fraction for cat albumin was 0.41. Elevation of hepatic venous pressure by 12.5 mmHg caused a fourfold increase in hepatic lymph flow with an increase in interstitial volume and a reduction in albumin exclusion. When the exclusion of heterologous (human) albumin was studied in the cat liver, much higher values were obtained than with homologous albumin. This effect may be due to polymerization of commercial human albumin on storage.

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Effect of Acute Elevation of Portal Venous Pressure on Mesenteric Blood Volume, Interstitial Fluid Volume and Hemodynamics

Circulation Research ◽

10.1161/01.res.6.5.592 ◽

1958 ◽

Vol 6 (5) ◽

pp. 592-599 ◽

Cited By ~ 47

Author(s):

EWALD E. SELKURT ◽

PAUL C. JOHNSON

Keyword(s):

Blood Volume ◽

Interstitial Fluid ◽

Venous Pressure ◽

Fluid Volume ◽

Portal Venous Pressure ◽

Interstitial Fluid Volume ◽

Acute Elevation

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Echinops Spp. Polysaccharide B Ameliorates Metabolic Abnormalities in a Rat Model of Type 2 Diabetes Mellitus

Current Topics in Nutraceutical Research ◽

10.37290/ctnr2641-452x.19:106-114 ◽

2020 ◽

Vol 19 (1) ◽

pp. 106-114

Author(s):

Guang Hao ◽

Xiaoyu Ma ◽

Mengru Jiang ◽

Zhenzhen Gao ◽

Ying Yang

Keyword(s):

Diabetes Mellitus ◽

Insulin Resistance ◽

Type 2 Diabetes ◽

Type 2 Diabetes Mellitus ◽

Insulin Secretion ◽

Insulin Receptor ◽

Skeletal Muscles ◽

Insulin Receptor Substrate ◽

Sprague Dawley

This study examined the in vivo effects of Echinops spp. polysaccharide B on type 2 diabetes mellitus in Sprague-Dawley rats. We constructed a type 2 diabetes mellitus Sprague-Dawley rat models by feeding a high-fat and high-sugar diet plus intraperitoneal injection of a small dose of streptozotocin. Using this diabetic rat model, different doses of Echinops polysaccharide B were administered orally for seven weeks. Groups receiving Xiaoke pill and metformin served as positive controls. The results showed that Echinops polysaccharide B treatment normalized the weight and blood sugar levels in the type 2 diabetes mellitus rats, increased muscle and liver glycogen content, improved glucose tolerance, increased insulin secretion, and reduced glucagon and insulin resistance indices. More importantly, Echinops polysaccharide B treatment upregulated the expression of insulin receptor in the liver, skeletal muscles, and pancreas, and significantly improved the expression levels of insulin receptor substrate-2 protein in the liver and pancreas, as well as it increased insulin receptor substrate-1 expression in skeletal muscles. These two proteins play crucial roles in increasing insulin secretion and in controlling type 2 diabetes mellitus. The findings of the present study suggest that Echinops polysaccharide B could improve the status of diabetes in type 2 diabetes mellitus rats, which may be achieved by improving insulin resistance. Our study provides a new insight into the development of a natural drug for the control of type 2 diabetes mellitus.

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Atrial Natriuretic Peptide as a Regulator of Transvascular Fluid Balance

Physiology ◽

10.1152/physiologyonline.1996.11.3.138 ◽

1996 ◽

Vol 11 (3) ◽

pp. 138-143 ◽

Cited By ~ 2

Author(s):

EM Renkin ◽

VL Tucker

Keyword(s):

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Plasma Volume ◽

Fluid Balance ◽

Interstitial Fluid ◽

Fluid Volume ◽

Interstitial Fluid Volume ◽

Atrial Natriuretic

Unlike other natriuretics, which act via the kidneys to reduce interstitial fluid volume with little change in plasma volume, atrial natriuretic peptide has important extrarenal actions that enable it to reduce plasma volume preferentially.

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Decreased vascular contractile and inositol phosphate responses in portal hypertensive rats

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y95-048 ◽

1995 ◽

Vol 73 (3) ◽

pp. 378-382 ◽

Cited By ~ 11

Author(s):

Yi-Tsau Huang ◽

Chuang-Ye Hong ◽

Pi-Chin Yu ◽

Ming-Fang Lee ◽

May C. M. Yang ◽

...

Keyword(s):

Portal Hypertension ◽

Contractile Response ◽

Inositol Phosphates ◽

Inositol Phosphate ◽

Venous Pressure ◽

Portal Vein Ligation ◽

Sprague Dawley ◽

Hypertensive Rats ◽

Contractile Responses ◽

Tail Artery

The purpose of this study was to investigate the vascular contractile and inositol phosphate responses in portal hypertensive rats. Portal hypertension was induced by partial portal vein ligation (PVL) in Sprague–Dawley rats. Sham-operated rats served as controls. Pressures, vasoconstrictor responses, and inositol phosphate responses were determined at 14 days after surgery. The portal venous pressure was significantly higher, while systemic arterial pressure and heart rate were lower, in PVL rats. Dose-dependent contractile responses were observed for both norepinephrine (1 × 10−8 – 3 × 10−6 M) and vasopressin (3 × 10−10 – 3 × 10−8 M) in the tail artery of both groups. The contractile response to norepinephrine was significantly decreased in PVL rats compared with controls at all doses. The contractile response to vasopressin was significantly decreased in PVL rats at higher doses. After myo-[3H]inositol incorporation in tail artery, the levels of 3H-labelled phosphatidylinositols (cpm/mg) were similar between the two groups. Norepinephrine (10−7 – 10−5 M) and vasopressin (10−10 – 10−8 M) dose dependently stimulated the 3H-labelled inositol phosphate production in the tail artery of both PVL and sham-operated rats. However, the response was significantly lower in PVL rats. The results suggested that the attenuation of vascular contractile responses in portal hypertension was reflected in the phosphoinositide messenger system.Key words: portal hypertension, inositol phosphates, phosphoinositide, tail artery, contractile response.

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Evaluation of renal and cardiovascular protection mechanisms of SGLT2 inhibitors: model-based analysis of clinical data

AJP Renal Physiology ◽

10.1152/ajprenal.00202.2018 ◽

2018 ◽

Vol 315 (5) ◽

pp. F1295-F1306 ◽

Cited By ~ 15

Author(s):

K. Melissa Hallow ◽

Peter J. Greasley ◽

Gabriel Helmlinger ◽

Lulu Chu ◽

Hiddo J. Heerspink ◽

...

Keyword(s):

Renal Impairment ◽

Clinical Data ◽

Healthy Subjects ◽

Interstitial Fluid ◽

Sglt2 Inhibitors ◽

Fluid Volume ◽

Diabetic Patients ◽

Pressure Reduction ◽

Physiological Variables ◽

Interstitial Fluid Volume

The mechanisms of cardiovascular and renal protection observed in clinical trials of sodium-glucose cotransporter 2 (SGLT2) inhibitors (SGLT2i) are incompletely understood and likely multifactorial, including natriuretic, diuretic, and antihypertensive effects, glomerular pressure reduction, and lowering of plasma and interstitial fluid volume. To quantitatively evaluate the contribution of proposed SGLT2i mechanisms of action on changes in renal hemodynamics and volume status, we coupled a mathematical model of renal function and volume homeostasis with clinical data in healthy subjects administered 10 mg of dapagliflozin once daily. The minimum set of mechanisms necessary to reproduce observed clinical responses (urinary sodium and water excretion, serum creatinine and sodium) was determined, and important unobserved physiological variables (glomerular pressure, blood and interstitial fluid volume) were then simulated. We further simulated the response to SGLT2i in diabetic virtual patients with and without renal impairment. Multiple mechanisms were required to explain the observed response: 1) direct inhibition of sodium and glucose reabsorption through SGLT2, 2) SGLT2-driven inhibition of Na+/H+ exchanger 3 sodium reabsorption, and 3) osmotic diuresis coupled with peripheral sodium storage. The model also showed that the consequences of these mechanisms include lowering of glomerular pressure, reduction of blood and interstitial fluid volume, and mild blood pressure reduction, in agreement with clinical observations. The simulations suggest that these effects are more significant in diabetic patients than healthy subjects and that while glucose excretion may diminish with renal impairment, improvements in glomerular pressure and blood volume are not diminished at lower glomerular filtration rate, suggesting that cardiorenal benefits of SGLT2i may be sustained in renally impaired patients.

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