Effects of adenosine and adenosine analogues on mean circulatory filling pressure and cardiac output in anesthetized rats

1997 ◽  
Vol 356 (1) ◽  
pp. 69-75 ◽  
Author(s):  
R. Tabrizchi
Keyword(s):  
Cardiac Output ◽  
Filling Pressure ◽  
Adenosine Analogues ◽  
Mean Circulatory Filling Pressure ◽  
Anesthetized Rats

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.

Possible equilibration of portal venous and central venous pressures during circulatory arrest

1993 ◽  
Vol 264 (1) ◽  
pp. H259-H261 ◽  
Author(s):  
R. Tabrizchi ◽  
S. L. Lim ◽  
C. C. Pang
Keyword(s):  
Circulatory Arrest ◽  
Venous Pressure ◽  
Filling Pressure ◽  
Intravenous Bolus ◽  
Ang Ii ◽  
Central Venous ◽  
Venous Tone ◽  
Mean Circulatory Filling Pressure ◽  
Anesthetized Rats ◽  
Total Body

The mean circulatory filling pressure technique has been used to assess total body venous tone. It involves measuring central venous pressure (CVP) at 5-8 s following circulatory arrest. This study examines if CVP and portal venous pressure (PVP) equilibrate when circulation is stopped by inflating a balloon implanted in the right atrium. CVP and PVP were measured in the control condition and after intravenous bolus injections of norepinephrine (NE, 1.6 microgram/kg), angiotensin II (ANG II, 1.3 microgram/kg), and isoproterenol (Iso, 0.5 microgram/kg) in conscious and pentobarbital-anesthetized rats. In conscious rats, CVP was similar to PVP after circulatory arrest under conditions of normal, elevated, or reduced vascular tone. In anesthetized rats, CVP was similar to PVP in the control condition and after intravenous bolus injection of NE and Iso but was less than PVP after the administration of ANG II. Therefore, mean circulatory filling pressure may not fully reflect total body venous tone in anesthetized, surgically stressed rats.

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.

Alpha 1- and alpha 2-adrenoceptor stimulation: changes in venous capacitance in intact dogs

1986 ◽  
Vol 250 (6) ◽  
pp. H1071-H1078
Author(s):  
C. P. Appleton ◽  
R. W. Lee ◽  
G. V. Martin ◽  
M. Olajos ◽  
S. Goldman
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Aortic Pressure ◽  
Filling Pressure ◽  
Venous Capacitance ◽  
Mean Circulatory Filling Pressure ◽  
Control Value ◽  
Circulatory Effects ◽  
Mean Aortic Pressure ◽  
Effective Vascular Compliance

The peripheral circulatory effects of alpha 1-adrenoceptor stimulation with methoxamine hydrochloride were compared with those of alpha 2-stimulation with UK 14304-18 in 12 intact dogs. Doses of each agent were infused to increase systemic vascular resistance and arterial pressure 50 and then 100% above control. Heart rate was controlled with atropine. At the higher dose, methoxamine increased mean aortic pressure (PAo) from a control of 77.3 +/- 1.6 to 152.9 +/- 3.2 mmHg, mean circulatory filling pressure (MCFP) from 8.0 +/- 0.4 to 13.3 +/- 1.3 mmHg, and central blood volume (CBV) from 21.3 +/- 1.1 to 25.9 +/- 1.5 ml X kg-1, whereas cardiac output did not change. UK 14304-18 increased PAo from 78.1 +/- 2.6 to 148.9 +/- 2.7 mmHg, MCFP from 7.9 +/- 0.4 to 10.6 +/- 0.4 mmHg, and CBV from 21.0 +/- 1.1 to 24.1 +/- 1.5 ml X kg-1, whereas cardiac output decreased from 151.7 +/- 9.4 to 126.3 +/- 5.8 ml X kg-1 X min-1. Mean circulatory filling pressure and CBV were higher with methoxamine than with UK 14304-18. Effective vascular compliance, determined by serial measurements of MCFP during ganglionic blockade after rapid changes in blood volume, decreased from a control value of 1.9 +/- 0.1 to 1.3 +/- 0.3 ml X mmHg-1 X kg-1 with methoxamine, but did not change with UK 14304-18 (1.9 +/- 0.1 ml X mmHg-1 X kg-1). At any given change in blood volume, there was a higher MCFP with alpha 1-stimulation compared with alpha 2-stimulation. Both agents decreased unstressed vascular volume.(ABSTRACT TRUNCATED AT 250 WORDS)

The pioneering use of systems analysis to study cardiac output regulation

2004 ◽  
Vol 287 (5) ◽  
pp. R1009-R1011 ◽  
Author(s):  
John E. Hall
Keyword(s):  
Cardiac Output ◽  
Systems Analysis ◽  
Output Regulation ◽  
Filling Pressure ◽  
Mean Circulatory Filling Pressure ◽  
Historical Significance ◽  
Classic Paper

This essay examines the historical significance of an APS classic paper that is freely available online: Guyton AC, Lindsey AW, and Kaufmann BN. Effect of mean circulatory filling pressure and other peripheral circulatory factors on cardiac output. Am J Physiol 180: 463-468, 1955 ( http://ajplegacy.physiology.org/cgi/reprint/180/3/463 ).

Hyperosmotic sodium salts reverse severe hemorrhagic shock: other solutes do not

1987 ◽  
Vol 253 (4) ◽  
pp. H751-H762 ◽  
Author(s):  
M. Rocha e Silva ◽  
I. T. Velasco ◽  
R. I. Nogueira da Silva ◽  
M. A. Oliveira ◽  
G. A. Negraes ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Survival Rates ◽  
Filling Pressure ◽  
Metabolic Effects ◽  
Plasma Sodium ◽  
Sodium Salts ◽  
Mean Circulatory Filling Pressure ◽  
Acid Base Equilibrium ◽  
Severe Hemorrhage

Severe hemorrhage in pentobarbital-anesthetized dogs (25 mg/kg) is reversed by intravenous NaCl (4 ml/kg, 2,400 mosmol/l, 98% long-term survival). This paper compares survival rates and hemodynamic and metabolic effects of hypertonic NaCl with sodium salts (acetate, bicarbonate, and nitrate), chlorides [lithium and tris(hydroxymethyl)aminomethane (Tris)], and nonelectrolytes (glucose, mannitol, and urea) after severe hemorrhage (44.5 +/- 2.3 ml/kg blood loss). Sodium salts had higher survival rates (chloride, 100%; acetate, 72%; bicarbonate, 61%; nitrate, 55%) with normal stable arterial pressure after chloride and nitrate; near normal cardiac output after sodium chloride; normal acid-base equilibrium after all sodium salts; and normal mean circulatory filling pressure after chloride, acetate, and bicarbonate. Chlorides and nonelectrolytes produced low survival rates (glucose and lithium, 5%; mannitol, 11%; Tris, 22%; urea, 33%) with low cardiac output, low mean circulatory filling pressure, and severe metabolic acidosis. Plasma sodium, plasma bicarbonate, mean circulatory filling pressure, cardiac output, and arterial pressure correlated significantly with survival; other parameters, including plasma volume expansion or plasma osmolarity, did not. It is proposed that high plasma sodium is essential for survival.

Influence of pregnancy on mean systemic filling pressure and the cardiac function curve in guinea pigs

1992 ◽  
Vol 70 (5) ◽  
pp. 669-674 ◽  
Author(s):  
S. C. Cha ◽  
G. W. Aberdeen ◽  
B. S. Nuwayhid ◽  
E. W. Quillen Jr.
Keyword(s):  
Cardiac Output ◽  
Pulmonary Artery ◽  
Cardiac Function ◽  
Blood Volume ◽  
Guinea Pigs ◽  
Venous Return ◽  
Filling Pressure ◽  
Right Atrial ◽  
Mean Circulatory Filling Pressure ◽  
Vascular Compliance

To assess the degree of circulatory fullness and to evaluate the influence of peripheral and cardiac factors in the regulation of cardiac output during pregnancy, the following studies were conducted using pentobarbital-anesthetized, open-chest nonpregnant and late term pregnant guinea pigs. Mean circulatory filling pressure was taken as the equilibrium pressure when the pulmonary artery was constricted. Total vascular compliance was assessed by ±5-mL changes in blood volume performed while this constriction was maintained. A separate group of guinea pigs was prepared with a pulmonary artery electromagnetic flow probe and right atrial catheter. Rapid infusion of saline was used to increase right atrial pressure while the cardiac output was determined. Pregnancy was characterized by the following changes relative to nonpregnant controls: 51Cr-labelled RBC blood volume increased from 55 ± 3 to 67 ± 3 mL/kg; mean circulatory filling pressure increased from 7.1 ± 0.2 to 8.0 ± 0.5 mmHg (1 mmHg = 133.322 Pa); right atrial pressure decreased from 3.4 ± 0.2 to 2.1 ± 0.3 mmHg; and cardiac output increased from 71.8 ± 3.9 to 96.8 ± 3.3 mL∙min−1∙kg−1. Total vascular compliance was not changed (2.1 ± 0.1 mL∙kg−1∙mmHg−1) and most of the expanded blood volume was accommodated as unstressed volume. The cardiac function curve was shifted upwards in pregnant animals. The resistance to venous return, as determined from the slope of the venous return curves, was not changed. These data suggest that the circulation of the pregnant guinea pig is slightly overfilled. The pressure gradient for venous return was increased, but a more important contribution to the increased levels of cardiac output is made by the increase in cardiac pumping ability.Key words: blood volume, mean circulatory filling pressure, vascular compliance, venous return.

Essential role of mean circulatory filling pressure in salt-induced hypertension

1979 ◽  
Vol 236 (1) ◽  
pp. R40-R47 ◽  
Author(s):  
R. D. Manning ◽  
T. G. Coleman ◽  
A. C. Guyton ◽  
R. A. Norman ◽  
R. E. McCaa
Keyword(s):  
Cardiac Output ◽  
Peripheral Resistance ◽  
Isotonic Saline ◽  
Filling Pressure ◽  
Initial Increase ◽  
Experimental Hypertension ◽  
Base Line ◽  
Plasma Aldosterone Concentration ◽  
Salt Loading ◽  
Mean Circulatory Filling Pressure

Experimental hypertension was produced in nine dogs by continuously infusing isotonic saline after renal mass had been surgically reduced to approximately 30% normal. Data were collected during 8 days of base-line measurements and 13 days of saline infusion to determine the cause of the initial increase in cardiac output observed in this type of hypertension and to measure other variables possibly important in the pathogenesis of hypertension. During the infusion period, these dogs demonstrated an increase in arterial pressure to hypertensive levels, transient increases in blood volume, sodium space, and cardiac output, initially depressed then subsequently elevated total peripheral resistance, and decreases in plasma renin activity and plasma aldosterone concentration. The mean circulatory filling pressure increased 4.7 Torr by day 3 and was still elevated 2 Torr at the end of the 2nd wk of infusion. We conclude that the initial increase in cardiac output in salt-loading hypertension is due to elevated fluid volumes and the associated increase in mean circulatory filling pressure.

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