Effects of freshwater and saltwater adaptation and dietary salt on fluid compartments, blood pressure, and venous capacitance in trout

2008 ◽  
Vol 294 (3) ◽  
pp. R1061-R1067 ◽  
Author(s):  
Kenneth R. Olson ◽  
Todd M. Hoagland
Keyword(s):  
Blood Pressure ◽  
Blood Volume ◽  
Extracellular Fluid ◽  
Filling Pressure ◽  
Salt Balance ◽  
Salt Loading ◽  
Mean Circulatory Filling Pressure ◽  
Vascular Capacitance ◽  
Fluid Compartments ◽  
The Relationship

Trout are of interest in defining the relationship between fluid and salt balance on cardiovascular function because they thrive in freshwater (FW; volume loading, salt depleting), saltwater (SW; volume depleting, salt loading), and FW while fed a high-salt diet (FW-HS; volume and salt loading). The effects of chronic (>2 wk) adaptation to these three protocols on blood volume (51Cr red cell space), extracellular fluid volume (99mTc-diethylene triaminepenta-acetic acid space), arterial (dorsal aortic; PDA) and venous (ductus Cuvier; Pven) blood pressure, mean circulatory filling pressure (zero-flow Pven), and vascular capacitance were examined in the present study on unanesthetized rainbow trout. Blood volume, extracellular fluid volume, PDA, Pven, and mean circulatory filling pressure progressively increased in the order SW < FW < FW-HS. Vascular capacitance in SW fish appeared to be continuous with the capacitance curve of FW fish and reflect a passive volume-dependent unloading of the venous system of FW fish. Vascular capacitance curves for FW-HS fish were displaced upward and parallel to those of FW fish, indicative of an active increase in unstressed blood volume without any change in vascular compliance. These studies are the first in any vertebrate to measure the relationship between fluid compartments and cardiovascular function during independent manipulation of volume and salt balance, and they show that volume, but not salt, balance is the primary determinant of blood pressure in trout. They also present a new paradigm with which to investigate the relative contributions of water and salt balance in cardiovascular homeostasis.

Role of β-adrenergic agonists in the control of vascular capacitance

1990 ◽  
Vol 68 (5) ◽  
pp. 575-585 ◽  
Author(s):  
Carl F. Rothe ◽  
A. Dean Flanagan ◽  
Roberto Maass-Moreno
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Peripheral Resistance ◽  
Filling Pressure ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Central Venous ◽  
Mean Circulatory Filling Pressure ◽  
Vascular Capacitance

The role of β-adrenergic agonists, such as isoproterenol, on vascular capacitance is unclear. Some investigators have suggested that isoproterenol causes a net transfer of blood to the chest from the splanchnic bed. We tested this hypothesis in dogs by measuring liver thickness, cardiac output, cardiopulmonary blood volume, mean circulatory filling pressure, portal venous, central venous, pulmonary arterial, and systemic arterial pressures while infusing norepinephrine (2.6 μg∙min−1∙kg−1), or isoproterenol (2.0 μg∙min−1∙kg−1), or histamine (4 μg∙min−1∙kg−1), or a combination of histamine and isoproterenol. Norepinephrine (an α- and β1-adrenergic agonist) decreased hepatic thickness and increased mean circulatory filling pressure, cardiac output, cardiopulmonary blood volume, total peripheral resistance, and systemic arterial and portal pressures. Isoproterenol increased cardiac output and decreased total peripheral resistance, but it had little effect on liver thickness or mean circulatory filling pressure and did not increase the cardiopulmonary blood volume or central venous pressure. Histamine caused a marked increase in portal pressure and liver thickness and decreased cardiac output, but it had little effect on the estimated mean circulatory filling pressure. Isoproterenol during histamine infusions reduced histamine-induced portal hypertension, reduced liver size, and increased cardiac output. We conclude that the β-adrenergic agonist, isoproterenol, has little influence on vascular capacitance or liver volume of dogs, unless the hepatic outflow resistance is elevated by agents such as histamine.Key words: β-adrenergic agonists, vascular capacitance, mean circulatory filling pressure, isoproterenol, histamine, liver sphincters.

Mean circulatory filling pressure: its meaning and measurement

1993 ◽  
Vol 74 (2) ◽  
pp. 499-509 ◽  
Author(s):  
C. F. Rothe
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Muscle Tone ◽  
Rapid Change ◽  
Circulatory System ◽  
Filling Pressure ◽  
The Body ◽  
Mean Circulatory Filling Pressure ◽  
Vascular Capacitance ◽  
The Mean

The volume-pressure relationship of the vasculature of the body as a whole, its vascular capacitance, requires a measurement of the mean circulatory filling pressure (Pmcf). A change in vascular capacitance induced by reflexes, hormones, or drugs has physiological consequences similar to a rapid change in blood volume and thus strongly influences cardiac output. The Pmcf is defined as the mean vascular pressure that exists after a stop in cardiac output and redistribution of blood, so that all pressures are the same throughout the system. The Pmcf is thus related to the fullness of the circulatory system. A change in Pmcf provides a uniquely useful index of a change in overall venous smooth muscle tone if the blood volume is not concomitantly changed. The Pmcf also provides an estimate of the distending pressure in the small veins and venules, which contain most of the blood in the body and comprise most of the vascular compliance. Thus the Pmcf, which is normally independent of the magnitude of the cardiac output, provides an estimate of the upstream pressure that determines the rate of flow returning to the heart.

Effects of nifedipine and captopril on vascular capacitance of ganglion-blocked anesthetized dogs

1990 ◽  
Vol 68 (3) ◽  
pp. 431-438 ◽  
Author(s):  
Richard I. Ogilvie ◽  
Danuta Zborowska-Sluis
Keyword(s):  
Cardiac Output ◽  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Blood Volume ◽  
Filling Pressure ◽  
Right Atrial ◽  
Central Blood Volume ◽  
Mean Circulatory Filling Pressure ◽  
Vascular Capacitance ◽  
Blood Volumes

The hemodynamic effects of nifedipine and captopril at doses producing similar reductions in arterial pressure were studied in pentobarbital- anesthetized ventilated dogs after splenectomy during ganglion blockade with hexamethonium. Mean circulatory filling pressure (Pmcf) was determined during transient circulatory arrest induced by acetylcholine at baseline circulating blood volumes and after increases of 5 and 10 mL/kg. Central blood volumes (pulmonary artery to aortic root) were determined from transit times, and separately determined cardiac outputs (right atrium to pulmonary artery) were estimated by thermodilution. Nifedipine (n = 5) increased Pmcf at all circulating blood volumes and reduced total vascular capacitance without a change in total vascular compliance. Central blood volume, right atrial pressure, and cardiac output were increased with induced increases in circulating blood volume. In contrast, captopril (n = 5) did not alter total vascular capacitance, central blood volume, right atrial pressure, or cardiac output at baseline or with increased circulating volume. Thus, at doses producing similar reductions in arterial pressure, nifedipine but not captopril increased venous return and cardiac output in ganglion-blocked dogs.Key words: mean circulatory filling pressure, vascular compliance, vascular capacitance, nifedipine, captopril.

Abstract 531: Regulation of Plasma 20-HETE and Soluble Epoxide Hydrolase by Salt Balance in Normotensive Subjects

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Fernando Elijovich ◽  
Nancy J Brown ◽  
Ginger L Milne ◽  
Cheryl L Laffer
Keyword(s):  
Blood Pressure ◽  
Epoxide Hydrolase ◽  
Direct Relationship ◽  
Soluble Epoxide Hydrolase ◽  
Salt Balance ◽  
Sodium Depletion ◽  
Salt Loading ◽  
Normotensive Subjects ◽  
Stimulation Of

The tissue sources of circulating and urinary 20-HETE and EETs are not well known. We have previously shown urine 20-HETE abnormalities in salt-sensitive (SS) hypertension. We studied plasma 20-HETE and EETs in normotensive volunteers classified as SS or salt resistant (SR) with an acute protocol of salt loading (HS, 460 mmol diet and iv) and depletion (LS, 10 mmol and furosemide). Plasma 20-HETE and total (EET+DHET) or active EET did not differ between SR and SS during baseline (B, UNaV 146±17 mmol/24hr), HS (422±20) or LS (24±6). In normal SR subjects, HS did not affect the levels of either eicosanoid but reduced degradation of EETs into DHETs by decreasing the activity of soluble epoxide hydrolase (sEH or DHET/[EET+DHET]). No major clinical or biochemical correlates for plasma 20-HETE were identified in B, HS or LS. In SR but not SS, EET+DHET (r=0.57, p<0.003) and DHET (r=0.45, p<0.03) correlated with aldosterone during B and HS. LS stimulated 20-HETE in both SS and SR and also unexpectedly increased EET+DHET in SR subjects. This did not lead to increased EETs because of concomitant stimulation of sEH with increased degradation into DHETs. In SR, stimulation of 20-HETE by LS correlated with greater natriuresis (r=0.71, p<0.02), greater reduction of MAP (r=0.66, p<0.03) and lesser stimulation of aldosterone (r=0.64, p<0.04), relationships not observed in SS. Finally, in SR subjects only, during B and HS, plasma 20-HETE correlated with the activity of sEH (r=0.56, p<0.005) and levels of DHET (r=0.63, p<0.001), but not with total or active EETs. Our data on stimulation of plasma 20-HETE by LS and its correlates (markers of severity of sodium depletion) suggest recruitment of systemic vasoconstrictor 20-HETE for maintenance of BP. Plasma EET responses to HS and LS are not consistent with its renal natriuretic role but correlate with aldosterone responses to salt balance, perhaps reflecting modulation of aldosterone actions on extrarenal ENaC. Although no significant correlations were detected between blood pressure and EETs, there was a direct relationship between plasma 20-HETE, sEH activity and degradation of EETs into DHETs. This suggests coordinated vasoconstriction and vasodilation by these eicosanoids in normal SR humans, which is disrupted in normotensive SS.

Reflex control of vascular capacitance during hypoxia, hypercapnia, or hypoxic hypercapnia

1990 ◽  
Vol 68 (3) ◽  
pp. 384-391 ◽  
Author(s):  
Carl F. Rothe ◽  
A. Dean Flanagan ◽  
Roberto Maass-Moreno
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Systemic Arterial Pressure ◽  
Filling Pressure ◽  
Venous Tone ◽  
Mean Circulatory Filling Pressure ◽  
Vascular Capacitance ◽  
The Mean

We tested the hypothesis that the changes in venous tone induced by changes in arterial blood oxygen or carbon dioxide require intact cardiovascular reflexes. Mongrel dogs were anesthetized with sodium pentobarbital and paralyzed with veruronium bromide. Cardiac output and central blood volume were measured by indocyanine green dilution. Mean circulatory filling pressure, an index of venous tone at constant blood volume, was estimated from the central venous pressure during transient electrical fibrillation of the heart. With intact reflexes, hypoxia (arterial Pao2 = 38 mmHg), hypercapnia (Paco2 = 72 mmHg), or hypoxic hypercapnia (Pao2 = 41; Paco2 = 69 mmHg) (1 mmHg = 133.32 Pa) significantly increased the mean circulatory filling pressure and cardiac output. Hypoxia, but not normoxic hypercapnia, increased the mean systemic arterial pressure and maintained the control level of total peripheral resistance. With reflexes blocked with hexamethonium and atropine, systemic arterial pressure supported with a constant infusion of norepinephrine, and the mean circulatory filling pressure restored toward control with 5 mL/kg blood, each experimental gas mixture caused a decrease in total peripheral resistance and arterial pressure, while the mean circulatory filling pressure and cardiac output were unchanged or increased slightly. We conclude that hypoxia, hypercapnia, and hypoxic hypercapnia have little direct influence on vascular capacitance, but with reflexes intact, there is a significant reflex increase in mean circulatory filling pressure.Key words: cardiovascular reflex, vascular capacitance, hypoxia, hypercapnia, mean circulatory filling pressure, venoconstriction.

Blood reservoir function in patients with Fontan circulation and asplenia syndrome

2019 ◽  
Vol 29 (8) ◽  
pp. 1016-1019
Author(s):  
Michitaka Fuse ◽  
Kenji Sugamoto ◽  
Seiko Kuwata ◽  
Rika Sekiya ◽  
Kohei Kawada ◽  
...  
Keyword(s):  
Blood Volume ◽  
Filling Pressure ◽  
Fontan Circulation ◽  
Splanchnic Circulation ◽  
Venous Capacitance ◽  
Mean Circulatory Filling Pressure ◽  
Hepatic Congestion ◽  
The Mean ◽  
Asplenia Syndrome ◽  
Blood Reservoir

AbstractSplanchnic circulation constitutes a major portion of the vasculature capacitance and plays an important role in maintaining blood perfusion. Because patients with asplenia syndrome lack this vascular bed as a blood reservoir, they may have a unique blood volume and distribution, which may be related to their vulnerability to the haemodynamic changes often observed in clinical practice. During cardiac catheterisation, the mean circulatory filling pressure was calculated with the Valsalva manoeuvre in 19 patients with Fontan circulation, including 5 patients with asplenia syndrome. We also measured the cardiac output index and circulatory blood volume by using a dye dilution technique. The blood volume and the mean circulatory filling pressure and the venous capacitance in patients with asplenia syndrome were similar to those in the remaining patients with Fontan circulation (85 ± 14 versus 77 ± 18 ml/kg, p = 0.43, 31 ± 8 versus 27 ± 5 mmHg, p = 0.19, 2.8 ± 0.6 versus 2.9 ± 0.9 ml/kg/mmHg, p = 0.86). Unexpectedly, our data indicated that patients with asplenia syndrome, who lack splanchnic capacitance circulation, have blood volume and venous capacitance comparable to those in patients with splanchnic circulation. These data suggest that (1) there is a blood reservoir other than the spleen even in patients with asplenia; (2) considering the large blood pool of the spleen, the presence of a symmetrical liver may represent the possible organ functioning as a blood reservoir in asplenia syndrome; and (3) if this is indeed the case, there may be a higher risk of hepatic congestion in patients with Fontan circulation with asplenia syndrome than in those without.

Urinary Excretion of 20-Hete, Natriuresis and Salt-Sensitivity of Blood Pressure in Essential Hypertension

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 716-716
Author(s):  
Cheryl L Laffer ◽  
Michal Laniado-Schwartzman ◽  
Mong-Heng Wang ◽  
Alberto Nasjletti ◽  
Fernando Elijovich
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Urinary Excretion ◽  
Salt Sensitivity ◽  
Nacl Transport ◽  
Salt Loading ◽  
Pm 10 ◽  
Salt Sensitive Hypertension ◽  
The Relationship ◽  
Na Depletion

P127 20-hydroxyeicosatetraenoic acid (20-HETE) inhibits NaCl transport in the loop of Henle. A deficit in its synthesis or action has been implicated in experimental salt-sensitive hypertension. We examined the relationship between urinary excretion of Na (UNaV) and 20-HETE in 26 essential hypertensive patients classified as salt-sensitive (SS=13) or resistant (SR=13) by an in-patient protocol of 24 hr salt-loading (HI: 160 mEq Na diet+2L saline iv) followed by 24-hr sodium deprivation (LO: 10 mEq Na diet+furosemide 120 mg in first 12 hrs). SS was defined as a fall in ambulatory systolic BP (SBP, noon to 10 pm)≥10 mmHg from HI to LO. The Table shows data in HI and in the second 12 hr period of LO, i.e., after Na depletion was achieved by furosemide. SS and SR did not differ in any of these data. 20-HETE did not correlate with race, age, or GFR. During HI, it showed a negative correlation with BMI (r=-0.44, p<0.03) and a positive one with BP (r=+0.42, p<0.04). Also, 20-HETE correlated with UNaV in all patients (r=+0.45, p<0.02), but this was due to a strong correlation in SR (r=+0.62, p<0.03), absent in SS. In LO, no correlations were observed between any of these measurements. Our data demonstrate that 20-HETE excretion varies with the state of salt-balance in human hypertension and diminishes with increasing obesity. Although excretion of 20-HETE is not different between SS and SR, there is a major difference in the relationship between excretion of this eicosanoid and natriuresis between these groups. Our data suggest that salt-sensitivity of blood pressure in human essential hypertension may result from impairment in a natriuretic mechanism dependent on 20-HETE.

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 Defining human mean circulatory filling pressure in the intensive care unit

2020 ◽  
Vol 129 (2) ◽  
pp. 311-316
Author(s):  
Marije Wijnberge ◽  
Jaap Schuurmans ◽  
Rob B. P. de Wilde ◽  
Martijn K. Kerstens ◽  
Alexander P. Vlaar ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Intensive Care Unit ◽  
Intensive Care ◽  
Venous Pressure ◽  
Filling Pressure ◽  
Central Venous ◽  
Venous Compliance ◽  
Icu Patients ◽  
Mean Circulatory Filling Pressure ◽  
Arterial Blood

In a cohort of 311 intensive care unit (ICU) patients, median mean circulatory filling pressure (Pmcf) measured after cardiac arrest was 15 mmHg (interquartile range 12–18). In 48% of cases, arterial blood pressure remained higher than central venous pressure, but correction for arterial-to-venous compliance differences did not result in clinically relevant alterations of Pmcf. Fluid balance, use of vasopressors or inotropes, and being on mechanical ventilation were associated with a higher Pmcf.

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