Changes In Extracellular Fluid Volume Research Articles

Dehydration: Isonatremic, Hyponatremic, and Hypernatremic Recognition and Management.

1. Karen S. Powers, MD, FCCM* 1. *Pediatric Critical Care, Golisano Children’s Hospital, University of Rochester School of Medicine, Rochester, NY. Clinicians need to recognize the signs and symptoms of dehydration to safely restore fluid and electrolytes. After completing this article, readers should be able to: 1. Understand that the signs and symptoms of dehydration are related to changes in extracellular fluid volume. 2. Recognize the different clinical and laboratory abnormalities in isonatremic, hyponatremic, and hypernatremic dehydration. 3. Know how to manage isonatremic dehydration. 4. Know how to manage hyponatremic dehydration. 5. Know how to manage hypernatremic dehydration. 6. Recognize how to avoid as well as treat complications of fluid and sodium repletion. 7. Understand which patients are candidates for oral rehydration. 8. Know the proper fluids and methods for oral rehydration. Dehydration is one of the leading causes of pediatric morbidity and mortality throughout the world. Diarrheal disease and dehydration account for 14% to 30% of worldwide deaths among infants and toddlers. (1) In the United States, as recently as 2003, gastroenteritis was the source for more than 1.5 million office visits, 200,000 hospitalizations, and 300 deaths per year. The rotavirus vaccine has significantly decreased the incidence of rotaviral gastroenteritis, and now norovirus is the leading cause in the United States. Water, which is essential for cellular homeostasis, comprises about 75% of body weight in infants and up to 60% in adolescents and adults. Without water intake, humans would die within a few days. (2) The human body has an efficient mechanism of physiologic controls to maintain fluid and electrolyte balance, including thirst. These mechanisms can be overwhelmed in disease states such as gastroenteritis because of rapid fluid and electrolyte losses, leading to dysnatremia, which is the most common electrolyte abnormality in hospitalized patients. (3) Infants and young children are …

Fluid overload, pulse wave velocity, and ratio of brachial pre-ejection period to ejection time in diabetic and non-diabetic chronic kidney disease.

Fluid overload is one of the characteristics in chronic kidney disease (CKD). Changes in extracellular fluid volume are associated with progression of diabetic nephropathy. Not only diabetes but also fluid overload is associated with cardiovascular risk factors The aim of the study was to assess the interaction between fluid overload, diabetes, and cardiovascular risk factors, including arterial stiffness and left ventricular function in 480 patients with stages 4–5 CKD. Fluid status was determined by bioimpedance spectroscopy method, Body Composition Monitor. Brachial-ankle pulse wave velocity (baPWV), as a good parameter of arterial stiffness, and brachial pre-ejection period (bPEP)/brachial ejection time (bET), correlated with impaired left ventricular function were measured by ankle-brachial index (ABI)-form device. Of all patients, 207 (43.9%) were diabetic and 240 (50%) had fluid overload. For non-diabetic CKD, fluid overload was associated with being female (β = –2.87, P = 0.003), heart disease (β = 2.69, P = 0.04), high baPWV (β = 0.27, P = 0.04), low hemoglobin (β = –1.10, P<0.001), and low serum albumin (β = –5.21, P<0.001) in multivariate analysis. For diabetic CKD, fluid overload was associated with diuretics use (β = 3.69, P = 0.003), high mean arterial pressure (β = 0.14, P = 0.01), low bPEP/ET (β = –0.19, P = 0.03), low hemoglobin (β = –1.55, P = 0.001), and low serum albumin (β = –9.46, P<0.001). In conclusion, baPWV is associated with fluid overload in non-diabetic CKD and bPEP/bET is associated with fluid overload in diabetic CKD. Early and accurate assessment of these associated cardiovascular risk factors may improve the effects of entire care in late CKD.

Measurement of leg fluid volume using bioelectrical impedance (1156.14)

Background: Fluid volume (FV) of body segments can be measured non‐invasively and continuously using bioelectrical impedance (BI). Electrical impedance of the cell membrane is high at low frequencies suggesting that BI using low frequencies will detect mainly extracellular fluid (ECF). The objective of this study was to determine relationships between leg FV measured using BI and changes in leg volume (LV) calculated geometrically.Methods: We measured FV between the knee and ankle using BI at low frequencies (50 &amp;amp; 100 KHz, Biopac) and leg circumferences at the knee, ankle and widest part of the calf in both legs of 7 healthy subjects (5 men, age 50.7±7.1 yrs, BMI 23.6±2.8 kg/m2). Measurements were made every 30 min while sitting for 4 hrs. LV was calculated geometrically by assuming a shape of a truncated cone. We also measured FV between the left knee and ankle every hour using a Xitron device that uses multiple frequencies up to 1 MHz to distinguish between ECF and intracellular fluid volumes. Paired t‐tests were used to compare changes (Δ) in Biopac FV (FV‐B) with ΔLV and Xitron measurements of ECF (ECF‐X) and total FV (TFV‐X).Findings: Relative to ΔLV, ΔFV‐B was lower in the first 2 hours of sitting (ΔLV 188.7±31.5, ΔFV‐B 79.8.9±121.3 ml, p&lt;0.0001) but similar between 2 and 4 hours (ΔLV 68.8±45.7 ml, ΔFV‐B 56.2±22.2 ml, p=0.50). In the left leg, all estimates of ΔFV‐B were consistent with ΔECF‐X and lower than ΔTFV‐X and ΔLV (at 4 hrs, ΔFV‐B 0.06±0.01 L, ΔECF‐X 0.06±0.01 L, ΔTFV‐X 0.08±0.07 L, ΔLV 0.14±0.04 L).Conclusions: FV measured using Biopac at low frequencies seems to quantify changes in ECF volume. Expansion of ECF volume accounts for only about half the volume expansion below the knees during the first 2 hours of sitting but accounts for most of it between 2 and 4 hours.

Is fluid overload more important than diabetes in renal progression in late chronic kidney disease?

Fluid overload is one of the major presentations in patients with late stage chronic kidney disease (CKD). Diabetes is the leading cause of renal failure, and progression of diabetic nephropathy has been associated with changes in extracellular fluid volume. The aim of the study was to assess the association of fluid overload and diabetes in commencing dialysis and rapid renal function decline (the slope of estimated glomerular filtration rate (eGFR) less than -3 ml/min per 1.73 m2/y) in 472 patients with stages 4-5 CKD. Fluid status was determined by bioimpedance spectroscopy method, Body Composition Monitor. The study population was further classified into four groups according to the median of relative hydration status (△HS =fluid overload/extracellular water) and the presence or absence of diabetes. The median level of relative hydration status was 7%. Among all patients, 207(43.9 %) were diabetic. 71 (15.0%) subjects had commencing dialysis, and 187 (39.6%) subjects presented rapid renal function decline during a median 17.3-month follow-up. Patients with fluid overload had a significantly increased risk for commencing dialysis and renal function decline independent of the presence or absence of diabetes. No significantly increased risk for renal progression was found between diabetes and non-diabetes in late CKD without fluid overload. In conclusion, fluid overload has a higher predictive value of an elevated risk for renal progression than diabetes in late CKD.

The use of bioimpedance spectroscopy to monitor response to treatment interventions with breast cancer-related lymphedema.

138 Background: Currently, limited tools are available to assess response to therapy in patients with breast cancer related lymphedema (BCRL). The purpose of this study was to perform an exploratory analysis to determine if, in clinical settings, bioimpedance spectroscopy (BIS) can detect changes in extracellular fluid volume in response to treatment of BCRL. Methods: Three centers that had experience with BIS (L-Dex U400, ImpediMed Limited, Brisbane, Australia) provided retrospective data on 50 patients with breast cancer who were evaluated with BIS at baseline and following loco-regional procedures. Patients had a pre-surgical L-Dex measurement as well as at least 2 post-surgical measurements (before and after BCRL intervention). Decisions regarding intervention were made by physicians with no L-Dex score cut-off utilized. An analysis was performed comparing changes in L-Dex scores for those patients undergoing treatment for BCRL (n=13) versus those not undergoing intervention (n=37). A second analysis was also performed on all patients with elevated L-Dex scores compared to baseline prior to intervention (n=32). Results: The mean age was 54 years old. Fifty four percent of patients underwent SLN biopsy with a mean of 7.9 nodes removed. The mean change in L-Dex score from baseline (pre-treatment) to the first post-surgical L-Dex score measurement was 3.3 +/- 6.8. When comparing the cohort treated for BCRL to those not treated, L-Dex scores were significantly reduced (-4.3 v. 0.1, p=0.005) following intervention. For the subset of patients with elevated L-Dex scores post-surgery, the change in L-Dex score following BCRL intervention was significantly reduced (-5.8 v. 0.1, p=0.001) compared with those observed. Conclusions: These results confirm that BIS can detect increases in L-Dex scores following breast surgery and can also detect reductions in L-Dex scores following intervention for early onset lymphedema. These results demonstrate that BIS has significant clinical utility as it can be used to monitor patients with early BCRL who undergo intervention and to follow these patients (through serial measurements) to document their short and long-term response to these treatments.

Change in extracellular fluid and arm volumes as a consequence of a single session of lymphatic massage followed by rest with or without compression

This study evaluated the acute effect of massage and compression components of lymphoedema treatment in women with and without arm lymphoedema secondary to breast cancer from a single treatment session. Women with (n = 15) and without (n = 15) lymphoedema underwent a single session of lymphatic massage. Following the session, women were randomised to receive or not receive a compression sleeve. Measurements were taken prior to, during, and following the massage as well as 30 min after completion of the massage. Bioimpedance spectrometry (BIS) was used to measure changes in extracellular fluid volume of all limbs as well as 10-cm segments within the upper limbs; perometry was used to measure changes in total upper limb volume as well as 10-cm segments within the limb. There were no significant changes after massage with or without compression. The median (and interquartile range) BIS ratios (unaffected:affected) for the whole upper limb for women with lymphoedema changed from 1.152 (1.053 to 1.422) to 1.192 (1.045 to 1.410) after massage, while the control group changed from 1.024 (0.998 to 1.047) to 1.041 (0.982 to 1.07). The median change in both the BIS ratio and the total arm volume measured with perometry from prior to the massage to following 30-min rest changed <2%, irrespective of whether women used a compression garment and whether women presented with or without lymphoedema. Examination of 10-cm segments within the arm also revealed no significant change in BIS ratio from one segment to the next. Massage alone or the application of compression after a single session of lymphatic massage was ineffective for reducing lymphoedema.

Do Changes in Relative Blood Volume Monitoring Correlate to Hemodialysis-Associated Hypotension?

Introduction: Intradialytic hypotension remains the most common complication for outpatient hemodialysis, and relative blood volume monitoring was designed to reduce hypotension. Reports of the usefulness of this technology, however, have been variable. Methods: We audited the usefulness of relative blood volume monitoring recorded throughout the mid-week dialysis in 72 stable adult outpatients who had multifrequency bioimpedance measurements. Results: The blood volume measurement (BVM) at the end of the session was 91.6 ± 0.6% and was not different from the nadir BVM recorded (90.7 ± 0.5). The BVM was strongly correlated with change in hematocrit (r = –0.56, p < 0.001) and albumin (r = –0.69, p < 0.001), but had no relationship with pre-, intra- or postdialysis blood pressure recordings. The BVM was not associated with ultrafiltration volume, but did correlate with a postdialysis change in extracellular fluid volume (r = –0.39, p = 0.006). Conclusion: In this audit, although the BVM at the end of the dialysis session was correlated with changes in hematocrit, serum albumin and extracellular fluid volume, the change in the relative BVM did not mirror changes in intradialytic blood pressure.

N-terminal proBNP—Marker of Cardiac Dysfunction, Fluid Overload, or Malnutrition in Hemodialysis Patients?

N-terminal probrain type natriuretic peptide (NTproBNP) has been proven to be a valuable biomarker for predicting cardiac events and mortality in the hemodialysis population. However recent reports have suggested that NTproBNP is a marker of volume overload rather than one of cardiac dysfunction. Therefore this study investigated the effect of fluid volume status on NTproBNP. Volume status was determined pre- and postdialysis in 72 stable hemodialysis outpatients by multifrequency bioimpedance, and the relationship to NTproBNP values was examined. The mean and median NTproBNP values were 931.9 +/- 230 and 242 (90 to 688) pmol/L, respectively. On simple correlation, NTproBNP was associated with markers of volume overload and cardiac dysfunction. However, on logistical regression analysis, the strongest association was with the predialysis ratio of extracellular water/total body water (beta 26.6, F29.6, P = 0.000), followed by postdialysis mean arterial blood pressure (beta 0.14, F17.1, P = 0.000), dialysate calcium concentration (beta -1.19, F14.1, P = 0.002), and change in extracellular fluid volume with dialysis (beta 0.27, F7.4, P = 0.009) In this study, NTproBNP was not associated with cardiac dysfunction as assessed by transthoracic echo or nuclear medicine scintigraphy but was dependent on factors associated with volume overload. However, because bioimpedance results can also be affected by malnutrition with loss of cell mass, NTproBNP may be elevated not only in patients with volume overload, but also those with malnutrition.

Rise in Extracellular Fluid Volume During High Sodium Depends on BMI in Healthy Men

A high sodium (HS) intake is associated to increased cardiovascular and renal risk, especially in overweight subjects. We hypothesized that abnormal sodium and fluid handling is involved, independent of hypertension or insulin resistance. Therefore, we studied the relation between BMI and sodium-induced changes in extracellular fluid volume (ECFV; distribution volume of (125)I-iothalamate) in 78 healthy men, not selected for BMI. A total of 78 subjects with a median BMI of 22.5 (range: 19.2-33.9 kg/m(2)) were studied after 1 week on a low sodium (LS) diet (50 mmol Na(+)/d) and after 1 week on HS (200 mmol Na(+)/d). The change from LS to HS resulted in an increase in ECFV of 1.2 +/- 1.8 l. Individual changes in ECFV were correlated to BMI (r = 0.361, P < 0.01). Furthermore, in response to HS, a higher BMI was associated to a higher rise in filtered load of sodium (FL(Na(+)) = [Na(+)] x GFR, r = 0.281, P < 0.05). Thus, a shift to HS leads to a larger rise in ECFV in healthy subjects with higher BMI, associated with an elevated FL(Na(+)) during HS. Although no hypertension occurred in these healthy subjects, our data provide a potential explanation for the interaction of sodium intake and BMI on cardiovascular and renal risk. Exaggerated fluid retention may be an early pathogenic factor in the cardiorenal complications of overweight.

Application of the sodium dilution principle to calculate extracellular fluid volume changes in horses during dehydration and rehydration

To apply the principle of sodium dilution to calculate the changes in the extracellular fluid (ECF) volume (ECFV) and intracellular fluid volume (ICFV) that occur during dehydration and rehydration in horses. 8 healthy horses of various breeds. Horses were dehydrated over 4 hours by withholding water and administering furosemide. Saline (0.9% NaCl) solution was administered IV during the next 2 hours (20 mL/kg/h; total 40 mL/kg). Horses were monitored for an additional hour following IV fluid administration. Initial ECFV was determined by use of multifrequency bioelectrical impedance analysis, and serum sodium concentration was used to calculate total ECF sodium content. Sodium and fluid volume losses were monitored and calculated throughout the study and used to estimate changes in ECFV and ICFV during fluid balance alterations. Changes during dehydration and rehydration primarily occurred in the ECFV. The sodium dilution principle estimated an overexpansion of the ECFV beyond the volume of fluid administered, indicating a small contraction of the ICFV in response to fluid administration. Serum and urinary electrolyte changes were recorded and were consistent with those of previous reports. The sodium dilution principle provided a simple method that can be used to estimate the changes in ECFV and ICFV that occur during fluid administration. Results suggested an overexpansion of the ECFV in response to IV saline solution administration. The sodium dilution principle requires further validation in healthy and clinically ill horses, which could provide clinical applications similar to those in other species.

Application of the sodium dilution principle to calculate extracellular fluid volume changes in horses during dehydration and rehydration

Application of the sodium dilution principle to calculate extracellular fluid volume changes in horses during dehydration and rehydration

Extracellular Fluid Volume in the Hypoalbuminemic Diabetic Patient

The number of people who have diabetes is increasing. Many develop significant complications associated with diabetes, such as neuropathy, retinopathy, and manifestations of cardiovascular disease. Overt diabetic nephropathy is diagnosed most often in patients who have longstanding diabetes and who develop hypertension, loss of renal function, peripheral edema, nephrotic range proteinuria, and hypoalbuminemia. This article discusses the changes in extracellular fluid volume in hypoalbuminemic patients who have diabetic nephropathy and changes in extracellular volume that occur in other forms of glomerular disease associated with hypoalbuminemia. This article also reviews the mechanisms responsible for hypoalbuminemia in proteinuric subjects who have chronic kidney disease.

Can Extracellular Fluid Volume Expansion in Hemodialysis Patients Be Safely Reduced Using the Hemocontrol Biofeedback Algorithm? A Randomized Trial

Extracellular fluid volume (ECFV) expansion in hemodialysis patients is associated with increased mortality. Attempts to remove excess fluid often result in intradialytic hypotension (IDH). Blood volume monitoring has been used to aid selection of ultrafiltration rates and dialysate conductivity to minimize IDH. Automating ultrafiltration and dialysate conductivity using the Hemocontrol Biofeedback System (HBS) has reduced IDH in IDH-prone subjects. We undertook a randomized controlled trial to determine if the HBS could safely reduce ECFV in ECF-expanded subjects. Patients with ECFV >45% of total body water were randomized to receive hemodialysis by either HBS or best clinical practices for 6 months. The primary endpoint was change in ECFV; exploratory variables included frequency of IDH, interdialytic weight gain, and changes in serum Na. Treatment with HBS did not result in any change in ECFV, even after multivariable adjustment. The frequency of IDH was however significantly lower with HBS when compared with best clinical practices without differences in other variables.

Frusemide results in an extracellular to intracellular fluid shift in horses

Frusemide (Lasix) is commonly used diuretic in horse racing and equine clinical practice. While pharmacology, pharmacodynamics, renal and haematological effects of frusemide have been studied in horses, its effects on the distribution of fluid within the horse remain unknown. To quantify the effects of frusemide on extracellular and intracellular fluid shifts. Horses were infused with 1 mg/kg body mass (n = 7) or 2 mg/kg (n = 9) i.v. frusemide. Total body water (TBW), extracellular fluid volume (ECFV) and plasma volume (PV) were measured using D2O, NaSCN and Evans blue dilution. Change in ECFV was assessed from the change in plasma [protein] and from repeated infusion/dilution of NaSCN. Frusemide resulted in a 0.020 +/- 0.002 l/kg decrease in TBW within 120 min. At 120 min after frusemide infusion the ECFV losses were nearly double the TBW losses, therefore ECFV loss in excess of TBW loss is seen as an increase in ICFV. Frusemide resulted in a net shift of fluid (electrolytes and water) from the extracellular to intracellular fluid compartment. The fluid shifts that occur within horses administered frusemide has not previously been characterised. The intracellular shift of fluid is of performance and clinical significance.

Modulation of single-nephron GFR in the db/db mouse model of type 2 diabetes mellitus

Hyperfiltration has been implicated in the progression toward diabetic nephropathy in type 2 diabetes mellitus (DM2). This study focuses for the first time on the in vivo modulation of single-nephron GFR (SNGFR) in the classic B6.Cg-m(+/+)Lepr(db)/J (db/db) mouse model of DM2. To obtain stable preparations, it was necessary to use a sustaining infusion of 3.3 ml.100 g body wt(-1) x h(-1), or higher. SNGFR (measured both proximally and distally) was greater in db/db vs. heterozygote (db/m) mice (P < 0.05) but not vs. the wild-type (WT) mice. The tubuloglomerular feedback (TGF) responses, determined as free-flow proximal vs. distal SNGFR differences, were significant in db/db mice (11.6 +/- 0.8 vs. 9.3 +/- 1.0 nl/min, P < 0.01), in db/m mice (8.0 +/- 0.8 vs. 7.2 +/- 0.6 nl/min, P < 0.02), and WT mice (9.9 +/- 0.6 vs. 8.9 +/- 0.7 nl/min, P < 0.05). After increasing the sustaining infusion in the db/db mice, to offset glycosuric urine losses, the SNGFR increased significantly, and the TGF response was abolished. In these volume-replete db/db mice, absolute fluid reabsorption measured both at the late proximal and distal tubular sites were significantly increased vs. db/m mice infused at 3.3 ml.100 g body wt(-1) x h(-1). After infusion of the neuronal nitric oxide synthase (nNOS) inhibitor S-methylthiocitrulline, SNGFR fell in both db/db and db/m mice. These studies show that SNGFR is elevated in this mouse model of DM2, is suppressed by nNOS inhibition, and is modulated by TGF influences that are altered by the diabetic state and responsive to changes in extracellular fluid volume.

Plasma sodium and hypertension

Dietary salt is the major cause of the rise in the blood pressure with age and the development of high blood pressure in populations. However, the mechanisms whereby salt intake raises the blood pressure are not clear. Existing concepts focus on the tendency for an increase in extracellular fluid volume (ECV), but an increased salt intake also induces a small rise in plasma sodium, which increases a transfer of fluid from the intracellular to the extracellular space, and stimulates the thirst center. Accordingly, the rise in plasma sodium is responsible for the tendency for an increase in ECV. Although the change in ECV may have a pressor effect, the associated rise in plasma sodium itself may also cause the blood pressure to rise. There is some evidence in patients with essential hypertension and the spontaneously hypertensive rat (SHR) that plasma sodium may be raised by 1 to 3 mmol/L. An experimental rise in sodium concentration greater than 5 mmol/L induces pressor effects on the brain and on the renin-angiotensin system. Such a rise can also induce changes in cultured vascular tissue similar to those that occur in the vessels of humans and animals on a high sodium diet, independent of the blood pressure. We suggest that a small increase in plasma sodium may be part of the mechanisms whereby dietary salt increases the blood pressure.

Volume natriuresis vs. pressure natriuresis.

Body fluid regulation depends on regulation of renal excretion. This includes a fast vasopressin-mediated water-retaining mechanism, and slower, complex sodium-retaining systems dominated by the renin-angiotensin aldosterone cascade. The sensory mechanisms of sodium control are not identified; effectors may include renal arterial pressure, renal reflexes, extrarenal hormones and other regulatory factors. Since the pioneering work of Guyton more than three decades ago, pressure natriuresis has been in focus. Dissociations between sodium excretion and blood pressure are explained as conditions where regulatory performance exceeds the precision of the measurements. It is inherent to the concept, however, that sudden transition from low to high sodium intake elicits an arterial pressure increase, which is reversed by the pressure natriuresis mechanism. However, such transitions elicit parallel changes in extracellular fluid volume thereby activating volume receptors. Recently we studied the orchestration of sodium homeostasis by chronic and acute sodium loading in normal humans and trained dogs. Small increases in arterial blood pressure are easily generated by acute sodium loading, and dogs appear more sensitive than humans. However, with suitable loading procedures it is possible - also acutely - to augment renal sodium excretion by at least one order of magnitude without any change in arterial pressure whatsoever. Although pressure natriuresis is a powerful mechanism capable of overriding any other controller, it seems possible that it is not operative under normal conditions. Consequently, it is suggested that physiological control of sodium excretion is neurohumoral based on extracellular volume with neural control of renin system activity as an essential component.

ADJUSTMENT OF DRY WEIGHT IN HEMODIALYSIS PATIENTS USING CONTINUOUS INTRADIALYTIC MEASUREMENT OF CALF MUL-TIFREQUENCY BIOIMPEDANCE

Background. Current concepts of dry weight (DW) prescription are largely based on clinical symptoms because of the difficulty in assessing extracellular fluid volume (ECV) during dialysis. We hypothesized that relative changes in extracellular resistance (Re)of the calf, expressed as [Re-o/Re-t], will become very low when ECV is contracted and individual DW is reached. Method. Continuous calf BIS was recorded repeatedly in 15 HD patients (n = 120). The first measurement was performed at clinical dry weight (CDW) as prescribed by the physician. Next measurements were made after post-HD body weight was gradually decreased by 0.2-0.3 kg per treatment. This procedure was iterated over several subsequent treatments until a treatment was observed where changes in Re-o/Re-t were <1 %. Weight at the end of this treatment was defined as “achieved dry weight (ADW)”. Results. Mean ADW (80.5 ± 34.1 kg) were significantly lower than CDW (81.4±32.0 kg, p <0.001). When ADW was achieved, pre-dialysis systolic blood pressure (SBP) was lower than at CDW (139.3±32.5 mmHg, vs. 129.4±33 mmHg, p<0.05), post-HD SBP did not differ. The incidence of clinical symptoms of underhydration was 15 % at CDW, but 46% at ADW. Conclusion. Continuous calf BIS during dialysis allows the assessment of changes in extracellular resistance as an indicator of changes in extracellular fluid volume. This method appears to be a promising new tool for the prediction of dry weight in hemodialysis patients.

Induction of c- fos in forebrain circumventricular organs after renal artery stenosis

Experiments were done in the anaesthetized rat to determine the effect of activation of renal receptors following renal arterial occlusion (RAO) on the induction of c- fos in neurons of the lamina terminalis in the forebrain. Following RAO, fos labeled neurons were found in both the subfornical organ (SFO) and the organum vasculosum of the lamina terminalis (OVLT). Transection of the renal nerves ipsilateral to RAO reduced (∼61%) the number of fos labeled neurons in the SFO and prevented the fos labeling in the OVLT. Similarly, administration of the angiotensin II converting enzyme inhibitor enalapril maleate prior to RAO also reduced (∼27%) the number of fos labeled neurons in the SFO to RAO. However, the number of fos labeled neurons was not altered in the OVLT. The number of fos labeled neurons in the SFO of the intact animals after RAO was found to be greater than the algebraic sum of the number of fos labeled neurons in the renal nerve transected and enalapril treated animals. These results suggest that neurons in the SFO are activated by at least two different mechanisms following renal artery occlusion; those involving the activation of afferent renal nerves and those due to changes in circulating levels of angiotensin II. In addition, afferent renal nerve inputs combined with the effect of increased circulating levels of angiotensin II produce a greater activation of the SFO than either input alone. On the other hand, the OVLT appears to be selectively activated by afferent renal nerve inputs following RAO. Taken together, these data suggest that neural inputs from the kidney may play an important role in controlling body fluid balance and arterial pressure (AP) by influencing the activity of forebrain circumventricular organs neurons that function in the detection of blood borne signals associated with changes in extracellular fluid volume.

Peripheral hyperosmolality reduces cardiac baroreflex sensitivity

The effects of acute increases in peripheral osmolality on cardiac baroreflex sensitivity were tested in conscious, unrestrained rats by fitting values for arterial blood pressure and heart rate during acute pressor and depressor responses to a four-parameter, sigmoid logistic function curve. Cardiac baroreceptor reflex function curves were produced before and following 30 min intravenous (i.v.) infusion of 2.5 M NaCl, an equipressor concentration of phenylephrine, isotonic saline, or 2.5 M NaCl following central administration of an angiotensin-converting enzyme (ACE) inhibitor. Hypertonic saline infusion increased blood pressure, reduced heart rate and baroreflex sensitivity (gain and range), and shifted the baroreflex function curve to a higher operating blood pressure. These effects were prevented or attenuated by prior central administration of an ACE inhibitor. Isotonic volume expansion did not alter baroreflex responses. Finally, phenylephrine produced similar changes in blood pressure but did not alter cardiac baroreflex responses. These data demonstrate that acute increases in peripheral osmolality and/or sodium decrease cardiac baroreflex sensitivity through generation of central angiotensin II, independent of changes in extracellular fluid volume and blood pressure.