scholarly journals Effects of endothelin-1 and homologous trout endothelin on cardiovascular function in rainbow trout

2000 ◽  
Vol 278 (2) ◽  
pp. R460-R468 ◽  
Author(s):  
Todd M. Hoagland ◽  
Leroy Weaver ◽  
J. Michael Conlon ◽  
Yugi Wang ◽  
Kenneth R. Olson
Keyword(s):  
Pressor Response ◽  
Venous Pressure ◽  
Cardiovascular Function ◽  
Cardiovascular Responses ◽  
Aortic Pressure ◽  
Systemic Resistance ◽  
Central Venous ◽  
Venous Compliance ◽  
Venous Infusion ◽  
Dose Dependent

The cardiovascular effects of endothelin (ET)-1 and the recently sequenced homologous trout ET were examined in unanesthetized trout, and vascular capacitance curves were constructed to evaluate the responsiveness of the venous system to ET-1. A bolus dose of 667 pmol/kg ET-1 doubled ventral aortic pressure; produced a triphasic pressor-depressor-pressor response in dorsal aortic pressure (PDA); increased central venous pressure, gill resistance, and systemic resistance; and decreased cardiac output, heart rate, and stroke volume. These responses were dose dependent. Bolus injection of trout ET (333 or 1,000 pmol/kg) produced essentially identical, dose-dependent cardiovascular responses as ET-1. Dorsal aortic infusion of 1 and 3 pmol ⋅ kg− 1 ⋅ min− 1ET-1 and central venous infusion into the ductus Cuvier of 0.3 and 1 pmol ⋅ kg− 1 ⋅ min− 1produced similar dose-dependent cardiovascular responses, although the increase in PDA became monophasic. The heightened sensitivity to central venous infusion was presumably due to the more immediate exposure of the branchial vasculature to the peptide. Infusion of 1 pmol ⋅ kg− 1 ⋅ min− 1ET-1 decreased vascular compliance but had no effect on unstressed blood volume. These results show that ETs affect a variety of cardiovascular functions in trout and that branchial vascular resistance and venous compliance are especially sensitive. The multiplicity of effectors stimulated by ET suggests that this peptide was extensively integrated into cardiovascular function early on in vertebrate phylogeny.

Effects of natriuretic peptides and nitroprusside on venous function in trout

1997 ◽  
Vol 273 (2) ◽  
pp. R527-R539 ◽  
Author(s):  
K. R. Olson ◽  
D. J. Conklin ◽  
A. P. Farrell ◽  
J. E. Keen ◽  
Y. Takei ◽  
...  
Keyword(s):  
Natriuretic Peptide ◽  
Natriuretic Peptides ◽  
Aortic Pressure ◽  
Systemic Resistance ◽  
Venous Compliance ◽  
Venous Capacitance ◽  
Unstressed Volume ◽  
Ventral Aorta

Active venous regulation of cardiovascular function is well known in mammals but has not been demonstrated in fish. In the present studies, the natriuretic peptides (NP) rat atrial natriuretic peptide (ANP) and trout ventricular natriuretic peptide (VNP), clearance receptor inhibitor SC-46542, and sodium nitroprusside (SNP) were infused into unanesthetized trout fitted with pressure cannulas in the ventral aorta, dorsal aorta, and ductus Cuvier, and a ventral aorta (VA) flow probe was used to measure cardiac output (CO). In another group, in vivo vascular (venous) capacitance curves were obtained during ANP or SNP infusion. The in vitro effects of NP on vessels and the heart were also examined. ANP, VNP, and SC-46542 decreased central venous pressure (PVen), CO, stroke volume (SV), and gill resistance (RG), whereas systemic resistance (RS) and heart rate (HR) increased. Dorsal aortic pressure (PDA) transiently increased and then fell even though RS remained elevated. ANP decreased mean circulatory filling pressure (MCFP), increased vascular compliance at all blood volumes, and increased unstressed volume in hypovolemic fish. ANP had no direct effect on the heart. ANP responses in vivo were not altered in trout made hypotensive by prior treatment with the angiotensin-converting enzyme inhibitor lisinopril. SNP reduced ventral aortic pressure (PVA), PDA, and RS, increased CO and HR, but did not affect PVen, SV, or RG. SNP slightly decreased MCFP but did not affect compliance or unstressed volume. In vitro, large systemic arteries were more responsive than veins to NP, whereas SNP relaxed both. These results show that, in vivo, NP decrease venous compliance, thereby decreasing venous return, CO, and arterial pressure. Conversely, SNP hypotension is due to decreased RS. This is the first evidence for active regulation of venous capacitance in fish, which probably occurs in small veins or venules. The presence of venous baroreceptors is also suggested.

Systemic filling pressure in intact circulation determined on basis of aortic vs. central venous pressure relationships

1994 ◽  
Vol 267 (6) ◽  
pp. H2255-H2258 ◽  
Author(s):  
E. A. Den Hartog ◽  
A. Versprille ◽  
J. R. Jansen
Keyword(s):  
Central Venous Pressure ◽  
Flow Resistance ◽  
Venous Pressure ◽  
Aortic Pressure ◽  
Filling Pressure ◽  
Central Venous ◽  
Mean Systemic Filling Pressure ◽  
Systemic Filling ◽  
The Mean ◽  
Systemic Filling Pressure

In the intact circulation, mean systemic filling pressure (Psf) is determined by applying a series of inspiratory pause procedures (IPPs) and using Guyton's equation of venous return (Qv) and central venous pressure (Pcv): Qv = a - b x Pcv. During an IPP series, different tidal volumes are applied to set Pcv at different values. From the linear regression between Qv and Pcv, Psf can be calculated as Psf = a/b. Guyton's equation can also be written as Qv = (Psf - Pcv)/Rsd, where Rsd is the flow resistance downstream of the places where blood pressure is equal to Psf. During an IPP, a steady state is observed. Therefore, we can also formulate the following equation for flow: Qs = (Pao - Psf)/Rsu, where Qs is systemic flow, Rsu is the systemic flow resistance upstream to Psf, and Pao is aortic pressure. Because both flows (Qs and Qv) are equal, it follows that Pao = Psf(1 + Rsu/Rsd) - Rsu/Rsd x Pcv. This equation implies a method to determine mean systemic filling pressure on the basis of Pao measurements instead of flow determinations. Using 22 IPPs in 10 piglets, we determined the mean systemic filling pressure, and we compared the values obtained from the flow curves with those obtained from the aortic pressure curves. The mean difference between the two methods was 0.03 +/- 1.16 mmHg. With the use of Pao measurements, the Psf can be estimated as accurately as in using flow determinations. The advantage of the new method is that estimation of cardiac output is not required.

Comparative responses to endothelin 2 and sarafotoxin 6b in systemic vascular bed of cats

1990 ◽  
Vol 258 (5) ◽  
pp. H1550-H1558
Author(s):  
R. K. Minkes ◽  
P. J. Kadowitz
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Venous Pressure ◽  
Cardiovascular Responses ◽  
Aortic Blood Flow ◽  
Vasodilator Activity ◽  
Pulmonary Arterial ◽  
Vascular Beds ◽  
Dose Dependent ◽  
Higher Doses

Cardiovascular responses to endothelin 2 (ET-2) and sarafotoxin 6b (S6b) were investigated in the cat. ET-2 (0.1-1 nmol/kg iv) decreased or elicited biphasic changes in arterial pressure (AP), whereas S6b (0.1-1 nmol/kg iv) only decreased AP. Central venous pressure (CVP), cardiac output (CO), and pulmonary arterial pressure (PAP) were increased. ET-2 produced biphasic changes in systemic vascular resistance (SVR), whereas S6b decreased SVR at the two lower doses and caused a biphasic change at the 1 nmol/kg dose. The effects of ET-1 and ET-2 were similar, whereas the effects of S6b were similar to ET-3. ET-2 and S6b had small effects on right ventricular contractile force and caused transient increases in heart rate. Distal aortic blood flow was increased in response to all doses of both peptides, whereas increases in carotid blood flow were observed only in response to the higher doses of ET-2 and S6b. ET-2 produced dose-dependent decreases in superior mesenteric artery (SMA) blood flow, whereas decreases in SMA flow in response to S6b were observed only at the 1 nmol/kg dose. Renal blood flow was decreased significantly only at the higher doses of ET-2 and S6b. The present data show that ET-2 and S6b can produce both vasodilation and vasoconstriction in the systemic and regional vascular beds of the cat and demonstrate previously unrecognized vasodilator activity in response to S6b. It is concluded that ET-2 and S6b produce complex cardiovascular responses in the anesthetized cat.

Cardiovascular responses to graded reductions in hindlimb perfusion in exercising dogs

1983 ◽  
Vol 245 (3) ◽  
pp. H481-H486 ◽  
Author(s):  
C. R. Wyss ◽  
J. L. Ardell ◽  
A. M. Scher ◽  
L. B. Rowell
Keyword(s):  
Heart Rate ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Work Load ◽  
Aortic Pressure ◽  
Aortic Flow ◽  
Nonlinear Relationship ◽  
All Speeds ◽  
The Relationship ◽  
High Work

In six dogs trained to run at 2, 4, and 6 mph, we caused graded reductions in hindlimb perfusion by compressing the terminal aorta. Our goal was to examine the relationship between hindlimb perfusion [terminal aortic flow (TAQ) and femoral arterial pressure (FP)] and cardiovascular responses [aortic pressure (AP), heart rate, and ascending aortic flow (CO)]. Small reductions in TAQ and FP produced bradycardia, small decreases in CO, and small increases in AP. Further reductions in TAQ and FP produced tachycardia, increased CO, and large increases in AP. AP rose by about 1 mmHg for each 1-mmHg fall in FP. The response was similar at all speeds, but as work load increased it required smaller reductions in FP and TAQ to cause a pressor response (e.g., at 6 mph we could not demonstrate a nonlinear relationship between TAQ and AP). At low work loads the cardiovascular responses to exercise were most likely set by signals other than feedback from exercising muscle because substantial reductions in hindlimb perfusion caused no significant cardiovascular responses. At moderate-to-high work loads or where muscle perfusion is restricted, metabolic feedback from muscle may play a role in cardiovascular responses to exercise.

Hepatic venous compliance and role of liver as a blood reservoir

1976 ◽  
Vol 231 (2) ◽  
pp. 292-295 ◽  
Author(s):  
WW Lautt ◽  
CV Greenway
Keyword(s):  
Central Venous Pressure ◽  
Blood Volume ◽  
Venous Pressure ◽  
Significant Proportion ◽  
Central Venous ◽  
Venous Compliance ◽  
Rapid Changes ◽  
Capacitance Vessels ◽  
Blood Reservoir

Changes in hepatic blood volume in response to rapid elevations in hepatic venous pressure were examined in cats using hepatic plethysmography. The liver was intact and received blood from an intact portal vein and hepatic artery. The hepatic blood volume increased in response to elevated venous pressure. Compliance of the hepatic capacitance vessels became greater as the distending venous pressure was increased over the range of venous pressures studied (0-9.4 mmHg). When hepatic venous pressure was elevated to 9.4 MMHg, the hepatic blood volume more than doubled. The liver serves as an important buffer for rapid changes in blood volume, the importance increasing with greater infused volumes of fluid. While overall venous compliance decreased at distending pressures in excess of 5-6 mmHg, the compliance of the hepatic capacitance vessels shows marked increases at pressures above this level. Expansions of the blood volume results in elevations of central venous pressure. Within a few minutes the hepatic capacitance vessels sequester a significant proportion of the added volume. As long as central venous pressure is raised, the liver demonstrates a secondary fluid buffering role by filtering large volumes of fluid across the vascular bed into the peritoneum.

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.

Role of venoconstriction in the cardiovascular responses of ducks to head immersion

1983 ◽  
Vol 244 (2) ◽  
pp. R292-R298
Author(s):  
B. L. Langille
Keyword(s):  
Cardiac Output ◽  
Central Venous Pressure ◽  
Venous Pressure ◽  
Venous Blood ◽  
Cardiovascular Responses ◽  
Energy Requirements ◽  
Similar Increase ◽  
Low Oxygen ◽  
Central Venous

Central venous pressure of ducks rose from resting values of 0.31 +/- 0.16 (SE) to 1.75 +/- 0.20 kPa during forced head immersion. Because a similar increase in mean circulatory pressure (Pmc) was also observed (0.71 +/- 0.16 to 2.15 +/- 0.20 kPa) the rise in central venous pressure was attributed to a venoconstrictor mechanism. When this venoconstrictor-induced rise in central venous pressure was prevented by graded withdrawal of venous blood, then immersion bradycardia was inhibited, and the reduced cardiac output associated with head immersion was largely the result of reduced stroke volume. When compared with normal dives, this intervention resulted in greater myocardial energy requirements, as assessed by the pressure-rate product. It is concluded that venoconstriction increases central venous pressure during head immersion. The increase in central venous pressure alters cardiac function through the Frank-Starling mechanism such that myocardial energy requirements are minimized during this period of low oxygen availability.

Short-term cardiovascular responses to a step decrease in peripheral conductance in humans

1994 ◽  
Vol 266 (1) ◽  
pp. H199-H211 ◽  
Author(s):  
K. Toska ◽  
M. Eriksen ◽  
L. Walloe
Keyword(s):  
Pressor Response ◽  
Venous Pressure ◽  
Cardiovascular Responses ◽  
Sudden Increase ◽  
Slow Increase ◽  
Cholinergic Blockade ◽  
Healthy Humans ◽  
Arterial Blood ◽  
Parasympathetic Bradycardia ◽  
Cardiac Stroke Volume

A step decrease in total peripheral conductance (TPC) was introduced in 10 healthy volunteers by rapid inflation to suprasystolic pressure of bilateral thigh cuffs. This provoked a sudden statistically significant increase in mean arterial blood pressure (MAP) of 5 mmHg during supine rest and of 8 mmHg during moderate supine exercise by the quadriceps muscles. Central venous pressure was not changed by cuff inflation. The increase in MAP was blunted by a rapid but transient decrease in both heart rate (HR) and cardiac stroke volume. At rest, a gradual increase in TPC, starting after 4 s, nearly fully restored MAP to its original value at 10 s. During exercise, MAP was halfway corrected at 10 s but then started to increase again, probably as a result of an ischaemic muscle pressor response. After cholinergic blockade by atropine, the immediate HR response was eliminated, but HR decreased gradually after a delay of 3 s. The time development of the slow increase in TPC was not changed by atropine. In conclusion, the regulatory correction of a sudden increase in arterial pressure in supine unanesthetized healthy humans is achieved through an immediate transient parasympathetic bradycardia during the first few seconds and a more gradual sympathetic peripheral vasodilation after 4 s. After cholinergic blockade, a slow presumably sympathetic HR response was observed.

Endurance training in dogs increases vascular responsiveness to an alpha 1-agonist

1988 ◽  
Vol 65 (2) ◽  
pp. 625-632 ◽  
Author(s):  
Y. M. Evans ◽  
J. N. Funk ◽  
J. B. Charles ◽  
D. C. Randall ◽  
C. F. Knapp
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Central Venous Pressure ◽  
Endurance Training ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Aortic Pressure ◽  
Central Venous ◽  
Vascular Responsiveness

The effects of endurance training on vascular responsiveness to an alpha 1-agonist and the associated changes in baroreflex modulation of heart rate and vascular resistance were studied. Graded dosages of phenylephrine were given to eight treadmill-trained dogs and to eight untrained dogs; both groups were chronically instrumented and were sedated and resting when tested. These dosages were repeated after ganglionic blockade. Aortic pressure, cardiac output, central venous pressure, peripheral resistance, and heart rate were each averaged over 30 s before injection and 90 s after injection. The slope of the peripheral resistance-dose relationship was significantly increased in trained compared with untrained dogs in both the unblocked and blocked cases [unblocked: trained 0.89, untrained 0.47; blocked: trained 4.30, untrained 2.05 (mmHg.l-1.min)/(microgram.kg-1)]. The unblocked resistance slopes were reduced with respect to the blocked slopes by 77 (untrained) and 79% (trained). The slope of the heart rate-aortic pressure response was reduced, but not significantly, by endurance training. We conclude that 6 wk of endurance training in dogs resulted in a doubling of the vascular responsiveness to an alpha 1-agonist, with no significant change in the baroreflex regulation of resistance or heart rate.

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