scholarly journals The 5‐HT 1A ‐receptor agonist, 8 OH‐DPAT, but not vasopressin, increases mean circulatory filling pressure in hypovolemic shock

2007 ◽  
Vol 21 (6) ◽  
Author(s):  
Ruslan L. Tiniakov ◽  
Karie E. Scrogin
Keyword(s):  
Receptor Agonist ◽  
Hypovolemic Shock ◽  
Filling Pressure ◽  
Mean Circulatory Filling Pressure

scholarly journals The spleen is required for 5-HT1A receptor agonist-mediated increases in mean circulatory filling pressure during hemorrhagic shock in the rat

2009 ◽  
Vol 296 (5) ◽  
pp. R1392-R1401 ◽  
Author(s):  
Ruslan Tiniakov ◽  
Karie E. Scrogin
Keyword(s):  
Metabolic Acidosis ◽  
Hemorrhagic Shock ◽  
Receptor Agonist ◽  
Blood Gases ◽  
Filling Pressure ◽  
Whole Body ◽  
Acid Base Balance ◽  
Acid Base ◽  
Mean Circulatory Filling Pressure ◽  
Base Balance

The 5-HT1A receptor agonist, 8- OH-DPAT, increases whole body venous tone (mean circulatory filling pressure; MCFP), and attenuates metabolic acidosis in a rat model of unresuscitated hemorrhagic shock. To determine whether improved acid-base balance was associated with sympathetic activation and venous constriction, MCFP, sympathetic activity (SA), and blood gases were compared in hemorrhaged rats following administration of 5-HT1A receptor agonist 8-OH-DPAT, the arterial vasoconstrictor arginine vasopressin (AVP), or saline. To further determine whether protection of acid-base balance was dependent on splenic contraction and blood mobilization, central venous pressure (CVP), MCFP, and blood gases were determined during hemorrhage and subsequent 8-OH-DPAT-administration in rats subjected to real or sham splenectomy. Subjects were hemorrhaged to an arterial pressure of 50 mmHg for 25 min and subsequently were treated with 8-OH-DPAT (30 nmol/kg iv), AVP titrated to match the pressor effect of 8-OH-DPAT (∼2 ng/min iv), or infusion of normal saline. 8-OH-DPAT increased MAP, CVP, MCFP, and SA, and decreased lactate accumulation. AVP did not affect CVP or SA, but raised MCFP slightly to a level intermediate between 8-OH-DPAT- and saline-treated rats. Infusion of AVP also produced a modest protection against metabolic acidosis. Splenectomy prevented the rise in CVP, MCFP, and protection against metabolic acidosis produced by 8-OH-DPAT but had no effect on the immediate pressor response to the drug. Together, the data indicate that 8-OH-DPAT produces a pattern of cardiovascular responses consistent with a sympathetic-mediated venoconstriction that is, in part, responsible for the drug's beneficial effect on acid-base balance. Moreover, blood mobilization stimulated by the spleen is required for the beneficial effects of 8-OH-DPAT.

Measurement of mean circulatory filling pressure and vascular compliance in domestic pigs

1990 ◽  
Vol 258 (6) ◽  
pp. H1925-H1932 ◽  
Author(s):  
R. I. Ogilvie ◽  
D. Zborowska-Sluis ◽  
B. Tenaschuk
Keyword(s):  
Cardiac Arrest ◽  
Circulatory Arrest ◽  
Filling Pressure ◽  
Right Atrial ◽  
Base Line ◽  
Pentobarbital Sodium ◽  
Closed Chest ◽  
Mean Circulatory Filling Pressure ◽  
Vascular Compliance ◽  
Venous Circulation

To measure mean circulatory filling pressure (Pmcf), a balloon was placed in the right atrium of seven pentobarbital sodium-anesthetized open-chest pigs for transient occlusion of flow combined with mechanical transfer of blood from the arterial to the venous circulation. Equilibration occurred within 6-8 s at a pressure at 12.3 +/- 0.3 (SE) mmHg after a 2.9 +/- 0.2 ml/kg transfer of blood. In another group of pentobarbital sodium-anesthetized closed-chest pigs, acetylcholine (ACh) was used to induce cardiac arrest. The Pmcf was 11.6 +/- 1.0 mmHg in the 7:17 pigs that arrested for 6-8 s. In four isoflurane-anesthetized closed-chest pigs, the Pmcf was 12.0 +/- 1.0 mmHg after terminal cardiac arrest induced by KCl. The pressure gradient for venous return [Pmcf--right atrial pressure (Pra)] averaged 5.9 +/- 0.2 mmHg. Total vascular compliance estimated from plots of Pmcf at base line, 5, and 10 ml/kg increases in circulating volume was 2.1 +/- 0.3 and 3.5 +/- 0.9 ml.kg-1.mmHg-1 in the balloon and ACh groups, respectively compared with 2.8 +/- 0.4 ml.kg-1.mmHg-1 using a volume infusion-withdrawal method without circulatory arrest. The use of ACh for the estimate of Pmcf in the pig is not recommended because of failure to consistently induce circulatory arrest and probable failure to achieve sufficient equilibrium of vascular pressures 6-8 s postarrest when it occurs.

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.

Central venous pressure and mean circulatory filling pressure in the dogfish Squalus acanthias: adrenergic control and role of the pericardium

2006 ◽  
Vol 291 (5) ◽  
pp. R1465-R1473 ◽  
Author(s):  
Erik Sandblom ◽  
Michael Axelsson ◽  
Anthony P. Farrell
Keyword(s):  
Central Venous Pressure ◽  
Venous Return ◽  
Venous Pressure ◽  
Filling Pressure ◽  
Control Fish ◽  
Central Venous ◽  
Venous Capacitance ◽  
Mean Circulatory Filling Pressure ◽  
Adrenergic Control ◽  
Venous Vasculature

Subambient central venous pressure (Pven) and modulation of venous return through cardiac suction (vis a fronte) characterizes the venous circulation in sharks. Venous capacitance was estimated in the dogfish S qualus acanthias by measuring the mean circulatory filling pressure (MCFP) during transient occlusion of cardiac outflow. We tested the hypothesis that venous return and cardiac preload can be altered additionally through adrenergic changes of venous capacitance. The experiments involved the surgical opening of the pericardium to place a perivascular occluder around the conus arteriosus. Another control group was identically instrumented, but lacked the occluder, and was subjected to the same pharmacological protocol to evaluate how pericardioectomy affected cardiovascular status. Routine Pven was negative (−0.08 ± 0.02 kPa) in control fish but positive (0.09 ± 0.01 kPa) in the pericardioectomized group. Injections of 5 μg/kg body mass ( Mb) of epinephrine and phenylephrine (100 μg/kg Mb) increased Pven and MCFP, whereas isoproterenol (1 μg/kg Mb) decreased both variables. Thus, constriction and relaxation of the venous vasculature were mediated through the respective stimulation of α- and β-adrenergic receptors. α-Adrenergic blockade with prazosin (1 mg/kg Mb) attenuated the responses to phenylephrine and decreased resting Pven in pericardioectomized animals. Our results provide convincing evidence for adrenergic control of the venous vasculature in elasmobranchs, although the pericardium is clearly an important component in the modulation of venous function. Thus active changes in venous capacitance have previously been underestimated as an important means of modulating venous return and cardiac performance in this group.

scholarly journals Estimating mean circulatory filling pressure in clinical practice: a systematic review comparing three bedside methods in the critically ill

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Marije Wijnberge ◽  
Daniko P. Sindhunata ◽  
Michael R. Pinsky ◽  
Alexander P. Vlaar ◽  
Else Ouweneel ◽  
...  
Keyword(s):  
Systematic Review ◽  
Clinical Practice ◽  
Critically Ill ◽  
Filling Pressure ◽  
Mean Circulatory Filling Pressure
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