scholarly journals Cerebrospinal fluid and interstitial fluid volume measurements in the human brain at 3T with EPI

2009 ◽  
Vol 61 (4) ◽  
pp. 834-841 ◽  
Author(s):  
Benjamin Bender ◽  
Uwe Klose
Keyword(s):  
Cerebrospinal Fluid ◽  
Human Brain ◽  
Interstitial Fluid ◽  
Fluid Volume ◽  
Interstitial Fluid Volume ◽  
Volume Measurements

Atrial Natriuretic Peptide as a Regulator of Transvascular Fluid Balance

Physiology ◽  
1996 ◽  
Vol 11 (3) ◽  
pp. 138-143 ◽  
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.

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

2018 ◽  
Vol 315 (5) ◽  
pp. F1295-F1306 ◽  
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.

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

1989 ◽  
Vol 257 (6) ◽  
pp. H2081-H2091 ◽  
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.

Relationship between interstitial fluid volume and pressure (compliance) in hypothyroid rats

2001 ◽  
Vol 281 (3) ◽  
pp. H1085-H1092 ◽  
Author(s):  
Helge Wiig ◽  
Tjøstolv Lund
Keyword(s):  
Skeletal Muscle ◽  
Peritoneal Dialysis ◽  
Thyroid Hormones ◽  
Interstitial Fluid ◽  
Experimental Situation ◽  
Fluid Pressure ◽  
Extracellular Fluid ◽  
Fluid Volume ◽  
The Body ◽  
Interstitial Fluid Volume

There is clinical and experimental evidence that lack of thyroid hormones may affect the composition and structure of the interstitium. This can influence the relationship between volume and pressure during changes in hydration. Hypothyrosis was induced in rats by thyroidectomy 8 wk before the experiments. Overhydration was induced by infusion of acetated Ringer, 5, 10, and 20% of the body weight, while fluid was withdrawn by peritoneal dialysis with hypertonic glucose. Interstitial fluid pressure (Pi) in euvolemia (euvolemic control situation) and experimental situation was measured with micropipettes connected to a servocontrolled counterpressure system. The corresponding interstitial fluid volume (Vi) was found as the difference between extracellular fluid volume measured as the distribution volume of 51Cr-labeled EDTA and plasma volume measured using125I-labeled human serum albumin. In euvolemia, Vi was similar or lower in the skin and higher in skeletal muscle of hypothyroid than in euthyroid control rats, whereas the corresponding Pi was higher in all tissues. During overhydration, Pi rose to the same absolute level in both types of rats, whereas during peritoneal dialysis there was a linear relationship between volume and pressure in all tissues and types of rats. Interstitial compliance (Ci), calculated as the inverse value of the slope of the curve relating changes in volume and pressure in dehydration, did not differ significantly in the hindlimb skin of hypothyroid and euthyroid rats. However, in skeletal muscle, Ci was 1.3 and 2.0 ml · 100 g−1 · mmHg−1 in hypothyroid and euthyroid rats ( P < 0.01), with corresponding numbers for the back skin of 2.7 and 5.0 ml · 100 g−1 · mmHg−1 ( P < 0.01). These experiments suggest that lack of thyroid hormones in rats changes the interstitial matrix, again leading to reduced Ci and reduced ability to mobilize fluid from the interstitium.

scholarly journals Edemagenic gain and interstitial fluid volume regulation

2008 ◽  
Vol 294 (2) ◽  
pp. R651-R659 ◽  
Author(s):  
R. M. Dongaonkar ◽  
C. M. Quick ◽  
R. H. Stewart ◽  
R. E. Drake ◽  
C. S. Cox ◽  
...  
Keyword(s):  
Fluid Balance ◽  
Interstitial Fluid ◽  
Fluid Pressure ◽  
Venous Hypertension ◽  
Fluid Volume ◽  
Balance Equations ◽  
Factors Affecting ◽  
Venous Circulation ◽  
Interstitial Fluid Volume ◽  
Simplifying Assumptions

Under physiological conditions, interstitial fluid volume is tightly regulated by balancing microvascular filtration and lymphatic return to the central venous circulation. Even though microvascular filtration and lymphatic return are governed by conservation of mass, their interaction can result in exceedingly complex behavior. Without making simplifying assumptions, investigators must solve the fluid balance equations numerically, which limits the generality of the results. We thus made critical simplifying assumptions to develop a simple solution to the standard fluid balance equations that is expressed as an algebraic formula. Using a classical approach to describe systems with negative feedback, we formulated our solution as a “gain” relating the change in interstitial fluid volume to a change in effective microvascular driving pressure. The resulting “edemagenic gain” is a function of microvascular filtration coefficient ( K f), effective lymphatic resistance ( R L), and interstitial compliance ( C). This formulation suggests two types of gain: “multivariate” dependent on C, R L, and K f, and “compliance-dominated” approximately equal to C. The latter forms a basis of a novel method to estimate C without measuring interstitial fluid pressure. Data from ovine experiments illustrate how edemagenic gain is altered with pulmonary edema induced by venous hypertension, histamine, and endotoxin. Reformulation of the classical equations governing fluid balance in terms of edemagenic gain thus yields new insight into the factors affecting an organ's susceptibility to edema.

Distribution volumes of [131I]albumin, [14C]sucrose, and 36Cl in sheep lung

1975 ◽  
Vol 39 (5) ◽  
pp. 773-779 ◽  
Author(s):  
S. L. Selinger ◽  
R. D. Bland ◽  
R. H. Demling ◽  
N. C. Staub
Keyword(s):  
Plasma Volume ◽  
Interstitial Fluid ◽  
Fluid Volume ◽  
The Body ◽  
Constant Infusion ◽  
Red Cell ◽  
Lung Water ◽  
Lung Weight ◽  
Interstitial Fluid Volume ◽  
Volumes Of Distribution

We measured the steady-state volumes of distribution for radioactive chloride, sucrose, and albumin in the lung of six anesthetized, spen-thorax sheep. We allowed 2 days for [131I]albumin to equilibrate throughout the body, 2 h for the 36Cl, and a 40-min constant infusion for [14C]sucrose before killing the animal. Five minutes before death, we gave [125I]albumin to tag lung plasma volume. We killed the animals by clamping both lung hila; we then removed the lungs and homogenized them. We measured residual red cell and plasma volume, total extravascular lung water, and the extravascular content of the three tracers. The distribution volumes expressed as fractions of blood-free lung weight were: 36Cl equals 0.44, sucrose equals 0.28, and albumin equals 0.07. If the sucrose distribution volume is taken as the best estimate of the lung's extravascular extracellular space, then chloride clearly overestimates the interstitial fluid volume, being either bound or partially intracellular. On the other hand, albumin clearly underestimates the interstitial fluid volume.

Effects of oestradiol-17β on testicular microcirculation in rats

1987 ◽  
Vol 115 (3) ◽  
pp. 489-495 ◽  
Author(s):  
A. Widmark ◽  
J. E. Damber ◽  
A. Bergh
Keyword(s):  
Blood Vessels ◽  
Interstitial Fluid ◽  
Fluid Volume ◽  
Polymorphonuclear Leucocytes ◽  
Testosterone Production ◽  
Interstitial Fluid Volume ◽  
Before And After ◽  
Testicular Steroidogenesis ◽  
Hypophysectomized Rats ◽  
Intact Rats

ABSTRACT The effect of oestradiol-17β on testicular micro-circulation in intact and hypophysectomized rats was studied before and after treatment with human chorionic gonadotrophin (hCG). Treatment of intact rats with oestradiol-17β for 5 days did not influence vasomotion but decreased testicular interstitial fluid volume (IFV). Treatment of intact rats with 50 IU hCG 8 h before the experiment began induced an increase in testicular IFV, abolished vasomotion and increased the accumulation of polymorphonuclear leucocytes in the testicular venules and interstitium. These changes were unaffected by pretreatment with oestradiol-17β, despite the decreased testosterone production. However, pretreatment with oestradiol-17β potentiated the hCG-induced migration of polymorphonuclear leucocytes to the interstitium. The interstitial fluid volume and number of polymor phonuclear leucocytes in blood vessels were decreased in hypophysectomized rats, and vasomotion was abolished. Daily treatment with 5 IU hCG increased the IFV and the number of polymorphonuclear leucocytes in blood vessels, and preserved vasomotion. Treatment of hypophysectomized rats with oestradiol-17β decreased testosterone production but did not influence basal IFV, vasomotion or the changes in IFV and vasomotion induced by 5 IU hCG. The present study shows that the regulation of testicular vascular permeability and vasomotion may not be directly related to testicular steroidogenesis, and that oestrogens are probably not involved as a mediator of the hCG-induced changes in testicular microcirculation. J. Endocr. (1987) 115, 489–495

Edema in Oral Mucosa after LPS or Cytokine Exposure

2006 ◽  
Vol 85 (5) ◽  
pp. 442-446 ◽  
Author(s):  
A. Bletsa ◽  
T. Nedrebø ◽  
K.J. Heyeraas ◽  
E. Berggreen
Keyword(s):  
Oral Mucosa ◽  
Interstitial Fluid ◽  
Fluid Pressure ◽  
Fluid Volume ◽  
Volume Distribution ◽  
Connective Tissues ◽  
Edema Formation ◽  
Necrosis Factor Alpha ◽  
Interstitial Fluid Volume ◽  
Tnf Α

Lowering of interstitial fluid pressure (Pif) is an important factor that explains the rapid edema formation in acute inflammation in loose connective tissues. Lipopolysaccharide (LPS) and the pro-inflammatory cytokines interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) are pathogenetic in gingivitis. To test if these substances induce lowering of Pif in rat oral mucosa, we measured Pif with a micropuncture technique. IL-1β and TNF-α caused lowering of Pif, whereas LPS induced an immediate increase in Pif, followed by lowering after 40 min. Measurements of fluid volume distribution showed a significant change in interstitial fluid volume (Vi) 1.5 hr after LPS exposure as Vi changed from 0.41 ± 0.02 to 0.51 ± 0.03 mL/g wet weight ( p < 0.05), confirming edema. These findings show that LPS, IL-1β, and TNF-α induce lowering of Pif in the rat oral mucosa and contribute to edema formation in LPS-induced gingivitis.

Sign in / Sign up

Export Citation Format

Share Document