Interstitial Correction of Blood Volume Decrease during Hemodialysis

1989 ◽  
Vol 12 (10) ◽  
pp. 626-631 ◽  
Author(s):  
P.M. Kouw ◽  
P.M.J.M. De Vries ◽  
P.L Oe
Keyword(s):  
Blood Pressure ◽  
Blood Volume ◽  
Extracellular Fluid ◽  
Compensatory Mechanism ◽  
Fluid Shift ◽  
Lower Blood ◽  
Volume Blood ◽  
Dialysate Sodium ◽  
Volume Decrease

The etiology of hypotension during hemodialysis is multifactorial. Probably a decrease in blood volume caused by ultrafiltration, and acetate are both involved, while refilling from the interstitium acts as a compensatory mechanism. An osmotically induced transcellular fluid shift to intracellular might reduce the refilling capacity. This study investigated the effect of ultrafiltration on blood volume, blood pressure and refilling. The role of acetate and blood volume decrease in hypotension was established and intra- and extracellular fluid changes were calculated. Blood volume decrease depended on ultrafiltration: at high ultrafiltration rates refilling failed, apparently more so at high acetate plasma levels. An isolated blood volume decrease did not lower blood pressure. Concomitant high acetate levels caused hypotension and also seemed to reduce refilling. Nearly all refilling fluid came from the extracelullar compartment. Only high dialysate sodium concentrations gave rise to an intracellular loss.

scholarly journals Positive and Negative Aspects of Sodium Intake in Dialysis and Non-Dialysis CKD Patients

Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 951
Author(s):  
Yasuyuki Nagasawa
Keyword(s):  
Blood Pressure ◽  
Nutritional Status ◽  
Water Intake ◽  
Salt Intake ◽  
Sodium Intake ◽  
Extracellular Fluid ◽  
Sodium Restriction ◽  
Dialysis Patients ◽  
Positive Effects ◽  
Volume Blood

Sodium intake theoretically has dual effects on both non-dialysis chronic kidney disease (CKD) patients and dialysis patients. One negatively affects mortality by increasing proteinuria and blood pressure. The other positively affects mortality by ameliorating nutritional status through appetite induced by salt intake and the amount of food itself, which is proportional to the amount of salt under the same salty taste. Sodium restriction with enough water intake easily causes hyponatremia in CKD and dialysis patients. Moreover, the balance of these dual effects in dialysis patients is likely different from their balance in non-dialysis CKD patients because dialysis patients lose kidney function. Sodium intake is strongly related to water intake via the thirst center. Therefore, sodium intake is strongly related to extracellular fluid volume, blood pressure, appetite, nutritional status, and mortality. To decrease mortality in both non-dialysis and dialysis CKD patients, sodium restriction is an essential and important factor that can be changed by the patients themselves. However, under sodium restriction, it is important to maintain the balance of negative and positive effects from sodium intake not only in dialysis and non-dialysis CKD patients but also in the general population.

scholarly journals Changes in Angiotensin Receptor Distribution and in Aortic Morphology Are Associated with Blood Pressure Control in Aged Metabolic Syndrome Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Verónica Guarner-Lans ◽  
Elizabeth Soria-Castro ◽  
Rocío Torrico-Lavayen ◽  
Araceli Patrón-Soberano ◽  
Karla G. Carvajal-Aguilera ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Renin Angiotensin System ◽  
Pressure Control ◽  
Premature Aging ◽  
Compensatory Mechanism ◽  
Histological Changes ◽  
Angiotensin System ◽  
Elevated Expression

The role of the renin-angiotensin system (RAS) in blood pressure regulation in MS during aging is unknown. It participates in metabolic syndrome (MS) and aging regulating vascular tone and remodeling. RAS might participate in a compensatory mechanism decreasing blood pressure and allowing MS rats to reach 18 months of age and it might form part of therapeutical procedures to ameliorate MS. We studied histological changes and distribution of RAS receptors in aortas of MS aged rats. Electron microscopy images showed premature aging in MS since the increased fibrosis, enlarged endothelium, and invasion of this layer by muscle cells that was present in control 18-month-old aortas were also found in 6-month-old aortas from MS rats. AT1, AT2, and Mas receptors mediate the effects of Ang II and Ang 1-7, respectively. Fluorescence from AT2 decreased with age in control and MS aortas, while fluorescence of AT1 increased in aortas from MS rats at 6 months and diminished during aging. Mas expression increased in MS rats and remained unchanged in control rats. In conclusion, there is premature aging in the aortas from MS rats and the elevated expression of Mas receptor might contribute to decrease blood pressure during aging in MS.

Significance of Increase in Labelled Albumin Disappearance Rate in Arterial Hypertension

1976 ◽  
Vol 51 (s3) ◽  
pp. 211s-213s
Author(s):  
M. Ulrych ◽  
Z. Ulrych
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Blood Volume ◽  
Plasma Renin ◽  
Disappearance Rate ◽  
Reference Standard ◽  
Hypertensive Patients ◽  
Volume Blood ◽  
Normotensive Subjects ◽  
Normotensive Control

1. Relationships between labelled albumin disappearance rate (LADR), plasma volume, blood volume, plasma renin activity (PRA) and blood pressure (BP) were studied in normotensive control subjects and patients with hypertension of different aetiology and severity. In essential hypertensive patients without complications an inverse linear relationship was found between blood pressure and plasma or blood volume. 2. Very close inverse correlations were found between LADR and PRA in both normotensive subjects and patients with uncomplicated essential hypertension. LADR appears to be an excellent reference standard for PRA. 3. It is postulated that LADR mainly reflects the relation between circulating fluid and vascular capacitance tone. LADR is increased in hypertension and blood volume may still be inappropriately high.

scholarly journals A reversal of fate : unravelling the role of central 5-HT in cardiorespiratory control in neonatal and adult rodents

2018 ◽  
Author(s):  
◽  
Jennifer Magnusson
Keyword(s):  
Blood Pressure ◽  
Physiological Role ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Autonomic Tone ◽  
Neurogenic Hypertension ◽  
Cardiorespiratory Control ◽  
Arterial Blood ◽  
Lower Blood

We seek to address the extent to which a specific loss of 5-hydroxytryptamine (5-HT) affects the control of respiration, arterial blood pressure (ABP) and heart rate (HR) across vigilance-states based on existing evidence suggesting that 5-HT defects increase the risk for Sudden Infant Death Syndrome (SIDS) and neurogenic hypertension. SIDS is the leading cause of infant mortality between 1 month and 1 year of age, occurs during sleep, and up to 70% of all SIDS cases have at least one 5-HT system abnormality. Neonatal rodents lacking central 5-HT exhibit severe apneas, and a reduced ABP and HR. Central 5-HT has been implicated in the etiology of neurogenic hypertension, presumably due to projections of 5-HT neurons within the midline raphe to vagal and presympathetic regions of the brain. However, data from studies examining the specific role of central 5-HT function is conflicting or inconclusive. Neurogenic hypertension accounts for more than 90% of all hypertensive cases and the normal fall in ABP that occurs during non-rapid eye movement sleep is absent in some patients with hypertension. Understanding the mechanisms associated with the development of hypertension is critical not only to lower blood pressure, but to lower its associated cardiovascular events. The purpose of this dissertation is to examine the role of central 5-HT in the control of ABP during sleep and reveal, mechanistically, the physiological role of 5-HT in the autonomic control of ABP in neonatal and adult rodents. The overarching hypothesis for this dissertation is that central 5-HT is required for the maintenance of ABP and autonomic tone at rest in both neonatal and adult rodents.

Vasopressin in the rat with spontaneous hypertension

1978 ◽  
Vol 235 (4) ◽  
pp. H361-H366 ◽  
Author(s):  
J. T. Crofton ◽  
L. Share ◽  
R. E. Shade ◽  
C. Allen ◽  
D. Tarnowski
Keyword(s):  
Blood Pressure ◽  
Urinary Excretion ◽  
Systolic Blood Pressure ◽  
Blood Volume ◽  
Rat Plasma ◽  
Wky Rats ◽  
Naturally Occurring ◽  
Plasma Vasopressin ◽  
Wistar Kyoto

Because vasopressin is one of the most potent naturally occurring pressor agents, and because of its importance in the regulation of blood volume and composition, we have undertaken a study of the role of vasopressin in the pathogenesis of the hypertension in the Okamoto-Aoki spontaneously hypertension (SH) rat. In SH rats, systolic blood pressure increased from 135 +/- 3 (SE) mmHg at age 33 days to 184 +/- 3 mmHg at age 75 days (P less than 0.01). In the Wistar-Kyoto (WKY) control rats, blood pressure increased from 100 +/- 2 to 120 +/- 2 mmHg (P less than 0.01). The differences in blood pressure between the SH and WKY rats at all ages were significant (P less than 0.01). During the age period 33-75 days, the 24-h urinary excretion of vasopressin in the SH rat was consistently more than twofold greater (P less than 0.01) than in the WKY rat. Plasma vasopressin concentration and pituitary vasopressin content were also elevated in the SH rat (P less than 0.01 and P less than 0.02, respectively). Changes in systolic blood pressure in the SH rat, however, were not paralleled by changes in the urinary excretion of vasopressin. The data indicate that the secretion of vasopressin is elevated in the SH rat. However, the magnitude of this elevation, in and of itself, may not be sufficient to account for the rising blood pressure in the young SH rat.

Evidence of Profiled Hemodialysis Efficacy in the Treatment of Intradialytic Hypotension

1998 ◽  
Vol 21 (7) ◽  
pp. 398-402 ◽  
Author(s):  
L. Colì ◽  
G. La Manna ◽  
V. Dalmastri ◽  
A. De Pascalis ◽  
G. Pace ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Volume ◽  
Sodium Concentration ◽  
Dialysis Session ◽  
Intradialytic Hypotension ◽  
Dialysis Patients ◽  
Non Invasive ◽  
Comparison Of The Results ◽  
Weight Decrease ◽  
Dialysate Sodium

In the last 10 years the percentage of dialysis patients suffering from clinical intradialytic intolerance has greatly increased. Profiled hemodialysis (PHD) is a new technical approach, alternative to standard hemodialysis (SHD) for the treatment of intradialytic symptomatic hypotension. It is based on intradialytic modulation of the dialysate sodium concentration, using a dialysate sodium concentration profile elaborated by a new mathematical kinetic model. The aim of PHD is to reduce the intradialytic blood volume decrease, thanks to a dialysate sodium profile, which allows a reduction in the plasma osmolarity decrease, thereby boosting intravascular fluid refilling. This work aims at clinically validating the PHD technique, by testing its ability, against SHD, to maintain a more stable intradialytic blood volume; this evaluation was supported by monitoring some hemodynamic parameters. Twelve dialysis patients on SHD treatment were selected because of their intradialytic symptomatic hypotension. Twelve SHD (one per patient) and 12 PHD sessions (one per patient) were performed to achieve the same sodium mass removal and body weight decrease on both PHD and SHD. During these sessions we monitored the blood volume variation % by the critline (a non invasive blood volume monitoring device), the mean blood pressure and heart rate directly and, finally, the stroke volume and cardiac output indirectly by bidimensional doppler-echocardiography. Comparison of the results obtained with the two techniques shows PHD to achieve a significantly more stable blood volume, blood pressure and cardiovascular function than SHD, in particular during the second and the third hour of the dialysis session.

Blood pressure maintenance in NHE3-deficient mice with transgenic expression of NHE3 in small intestine

2005 ◽  
Vol 288 (3) ◽  
pp. R685-R691 ◽  
Author(s):  
William T. Noonan ◽  
Alison L. Woo ◽  
Michelle L. Nieman ◽  
Vikram Prasad ◽  
Patrick J. Schultheis ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Small Intestine ◽  
Transgenic Expression ◽  
Specific Effects ◽  
Lower Blood ◽  
Blood Pressures ◽  
Pressure Natriuresis ◽  
Deficient Mice ◽  
Robust Response

NHE3 Na+/H+ exchanger knockout ( Nhe3−/−) mice have severe absorptive deficits in the kidney proximal tubule and intestinal tract. The resulting hypovolemia has confounded efforts to carefully evaluate the specific effects of NHE3 deficiency on kidney function. Development of mice with transgenic expression of NHE3 in the small intestine (tg Nhe3−/−) has allowed us to analyze the role of renal NHE3 in overall maintenance of blood pressure, pressure natriuresis, and autoregulation of both glomerular filtration rate (GFR) and renal blood flow (RBF). Ambulatory blood pressure, measured by telemetry, was lower in tg Nhe3−/− mice than in wild-type controls (tg Nhe3+/+) when the mice were maintained on a normal NaCl diet but was normalized when they were provided with a high NaCl intake. Furthermore, administration of the AT1-receptor blocker losartan showed that circulating ANG II plays a major role in maintaining blood pressure in tg Nhe3−/− mice fed normal NaCl but not in those receiving high NaCl. Clearance studies revealed a blunted pressure-natriuresis response in tg Nhe3−/− mice at lower blood pressures but a robust response at higher blood pressures. Autoregulation of GFR and RBF was normal in tg Nhe3−/− mice. These results show that dietary NaCl loading normalizes blood pressure in awake tg Nhe3−/− mice and that alterations in NHE3 activity are not essential for normal autoregulation of GFR and RBF. Furthermore, the data strongly support the hypothesis that NHE3 plays an important role in the diuretic and natriuretic responses to increases in blood pressure but also show that mechanisms not involving NHE3 mediate pressure natriuresis in the higher range of blood pressures studied.

Lesions of A1 noradrenergic cells affect AVP release and heart rate during hemorrhage

1987 ◽  
Vol 253 (5) ◽  
pp. H1012-H1017 ◽  
Author(s):  
G. A. Head ◽  
A. W. Quail ◽  
R. L. Woods
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Volume ◽  
Ventrolateral Medulla ◽  
Sham Operation ◽  
Noradrenergic Neurons ◽  
Reflex Tachycardia ◽  
Conscious Rabbits ◽  
Plasma Arginine

The role of A1 noradrenergic cells of the ventrolateral medulla in the changes in mean arterial pressure (MAP), heart rate (HR), and plasma arginine vasopressin (AVP) after slow continuous hemorrhage (2% blood vol/min up to 35%) was examined by comparing responses in conscious rabbits before and 3 wk after a sham operation or A1 lesions. In the control experiments, MAP fell minimally up to the withdrawal of 20% of blood volume after which it fell abruptly to 20-30 mmHg below control by the 35% level. Plasma AVP increased nonlinearly during progressive hemorrhage with significant increases occurring only after 25% of blood volume was removed. In contrast, HR increased linearly after the onset of bleeding. After A1 lesions, which destroyed 84% (range 80-94%) of the noradrenergic cells, the amount of AVP released and the tachycardia during hemorrhage were reduced by 83 and 61%, respectively (P less than 0.005), but the fall in MAP was minimally affected. Basal values of MAP, HR, or plasma AVP were not affected by the lesions. These results suggest that during hemorrhage in conscious rabbits A1 noradrenergic neurons are important for the secretion of AVP and the reflex tachycardia but play little role in the maintenance of blood pressure.

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