Hemodynamic responses to acute volume expansion in Dahl salt-sensitive rats

1991 ◽  
Vol 260 (1) ◽  
pp. R32-R38
Author(s):  
R. S. Reddy ◽  
C. Baylis ◽  
T. A. Kotchen
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Volume Expansion ◽  
Peripheral Resistance ◽  
Extracellular Fluid ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Hemodynamic Responses ◽  
Cardiopulmonary Baroreflex

The purpose of this study is to evaluate hemodynamic responses to acute volume expansion in chronically instrumented, conscious Dahl salt-sensitive (Dahl-S) and Dahl salt-resistant (Dahl-R) rats that have been maintained on either 0.45% NaCl, 1% NaCl, or 7% NaCl (5 days) intakes. Total peripheral resistance (TPR), but not arterial pressure, was increased by 5 days of 7% NaCl in Dahl-S (P less than 0.05) but not in Dahl-R. In Dahl-S, but not in Dahl-R, right atrial pressure increased with increasing dietary NaCl (P less than 0.05). On the 0.45% NaCl intake, atrial pressure did not differ in the two strains, whereas on both the 1 and 7% NaCl diets atrial pressure was higher in Dahl-S than in Dahl-R (P less than 0.05). In response to acute extracellular fluid volume expansion, arterial pressure did not change, and cardiac output increased in Dahl-S and in Dahl-R. On the 0.45% NaCl intake, TPR decreased (P less than 0.01) similarly in response to volume expansion in both strains; however, on the 1% NaCl intake TPR decreased in Dahl-R (P less than 0.05) but not in Dahl-S. In contrast, in animals fed 7% NaCl for 5 days, TPR decreased acutely in Dahl-S (P less than 0.01) but not in Dahl-R. These observations suggest that cardiopulmonary baroreflex activity is impaired in Dahl-S on a 1% NaCl intake, possibly as a consequence of elevated right atrial pressure. This alteration of the cardiopulmonary baroreflex may contribute to increased TPR in Dahl-S on a high-NaCl intake.

Hemodynamic studies in DOCA-salt hypertensive rats after opening of an arteriovenous fistula

1992 ◽  
Vol 262 (6) ◽  
pp. H1802-H1808 ◽  
Author(s):  
M. Huang ◽  
R. L. Hester ◽  
A. C. Guyton ◽  
R. A. Norman
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Hypertensive Rats

We determined the cardiovascular responses in normal and deoxycorticosterone acetate (DOCA)-salt hypertensive rats with reduced total peripheral resistance due to an arteriovenous (a-v) fistula. Animals were divided into four groups: control, fistula, DOCA-salt, and DOCA-salt fistula. The fistula was made by anastomosing the aorta and vena cava below the renal arteries. Four weeks after the creation of the fistula both DOCA-salt and DOCA-salt fistula animals received DOCA and salt for 6–8 wk. At the end of 10–12 wk we measured mean arterial pressure, cardiac output, tissue flows, and right atrial pressure. Flow measurements using radioactive microspheres were made in anesthetized animals. Cardiac index (CI) was 202% higher in the fistula group than in the control animals and 165% higher in the DOCA-salt fistula than in the DOCA-salt animals. There was no difference in cardiac output between the control and DOCA-salt animals. The increase in cardiac output was due to the fistula flow as evidenced by a significant increase in the number of microspheres in the lung. Mean arterial pressure was 115 +/- 4 mmHg (control) and 108 +/- 5 mmHg (fistula) in non-DOCA rats but increased in both DOCA groups, 159 +/- 3 mmHg (DOCA-salt) and 145 +/- 5 mmHg (DOCA-salt fistula). Right atrial pressure was increased above control in both fistula animals but was normal in DOCA-salt animals. Total peripheral resistance (TPR) was higher than control in DOCA-salt animals, but TPR in both the fistula and DOCA-salt fistula animals was lower than control.(ABSTRACT TRUNCATED AT 250 WORDS)

Atriopeptin II lowers cardiac output in conscious sheep

1985 ◽  
Vol 249 (6) ◽  
pp. R776-R780 ◽  
Author(s):  
B. A. Breuhaus ◽  
H. H. Saneii ◽  
M. A. Brandt ◽  
J. E. Chimoskey
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Smooth Muscle ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure

Atrial natriuretic peptides cause natriuresis, kaliuresis, diuresis, and hypotension. They relax vascular smooth muscle in vitro, and they dilate renal vessels in vivo. Hence, we tested the hypothesis that they produce hypotension by lowering total peripheral resistance. The studies were performed in conscious chronically instrumented sheep standing quietly in their cages. Atriopeptin II (AP II) was infused into the right atrium for 30 min at 0.1 nmol X kg-1 X min-1. Atriopeptin II lowers arterial pressure (9%, P less than 0.05) by lowering cardiac output (18%, P less than 0.05), stroke volume (28%, P less than 0.05), and right atrial pressure (2.3 mmHg, P less than 0.05). Heart rate and total peripheral resistance increase (16 and 13%, respectively, P less than 0.05). Partial ganglionic blockade with trimethaphan camsylate during AP II infusion prevents the increases in heart rate and total peripheral resistance. The changes in right atrial pressure, stroke volume, and cardiac output persist, and arterial pressure falls further (27%, P less than 0.05). These hemodynamic data are consistent with direct AP II-induced relaxation of venous smooth muscle with reduction of venous return, right atrial pressure, stroke volume, cardiac output, and arterial pressure, followed by reflex activation of the sympathetic nervous system to increase heart rate and total peripheral resistance. Because partial ganglionic blockade alone and AP II alone cause similar reductions in right atrial pressure (2.1 and 2.3 mmHg, respectively) but AP II causes a greater fall in stroke volume (28 vs. 13%), it is possible that AP II also causes coronary vasoconstriction.

Cardiovascular function and norepinephrine-thermogenesis in cold-acclimatized rats

1963 ◽  
Vol 204 (5) ◽  
pp. 888-894 ◽  
Author(s):  
Eugene Evonuk ◽  
John P. Hannon
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Room Temperature ◽  
Metabolic Response ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Systemic Resistance

The cardiovascular and metabolic actions of norepinephrine (NE) and their inter-relationships were studied at normal room temperature in anesthetized, warm-acclimatized (W-A) (26 ± 1 C) and cold-acclimatized (C-A) (3 ± 1 C) rats. The cardiac output, heart rate, stroke volume, arterial pressure, right atrial pressure, and systemic resistance were measured prior to NE infusion; during NE infusion (2 µg/min) at the 25, 50, 75, and 100% levels of increased metabolism; and after infusion of NE had ceased. Norepinephrine caused a greater increase in the cardiac output, heart rate, stroke volume, and right atrial pressure in the C-A animals than it did in W-A animals. During the early metabolic response to NE (i.e., up to 25% increase in O2 consumption) there was a marked increase in the arterial pressure of both W-A and C-A rats, with the latter showing the greater maximum response. Beyond the 25% level of increased metabolism the arterial pressure and concomitantly the systemic resistance of the C-A animals declined sharply to the preinfusion levels where they remained throughout the course of infusion. In contrast to this, the arterial pressure and systemic resistance of the W-A animals remained high. It was concluded that norepinephrine-calorigenesis in the C-A rat is supported by a greater capacity to increase the cardiac output and an ability to preferentially reduce the systemic resistance to actively metabolizing areas (i.e., the viscera).

Vagally mediated regulation of renal function in conscious primates

1986 ◽  
Vol 250 (4) ◽  
pp. H546-H549
Author(s):  
S. F. Vatner ◽  
W. T. Manders ◽  
D. R. Knight
Keyword(s):  
Renal Function ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Rhesus Monkeys ◽  
Volume Expansion ◽  
Urine Flow ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Water Excretion

The effects of vagal denervation (VD) were examined on responses of Na+ and water excretion to acute volume expansion (18 ml/kg of 6% dextran in saline) in six conscious rhesus monkeys with chronic sinoaortic denervation (SAD). After SAD, volume expansion increased mean arterial pressure (from 95 +/- 6.6 to 119 +/- 7.5 mmHg), right atrial pressure (from 1.3 +/- 0.7 to 5.9 +/- 1.8 mmHg), urine flow (from 0.08 +/- 0.01 to 0.68 +/- 0.20 ml/min), and Na+ excretion (from 1.30 +/- 0.45 to 29.51 +/- 10.40 mueq/min). After VD, volume expansion increased mean arterial and right atrial pressures similarly, but induced significantly lower (P less than 0.05) increases in urine flow (from 0.05 +/- 0.01 to 0.19 +/- 0.03 ml/min) and Na+ excretion (from 0.87 +/- 0.27 to 11.50 +/- 6.13 mueq/min). Thus vagal mechanisms appear to play an important role in mediating excretion of Na+ and water in response to acute volume expansion in the conscious primate.

Diversion of blood flow from noncompliant to compliant vasculature in awake dogs: mechanical impact on right atrial pressure

2006 ◽  
Vol 290 (1) ◽  
pp. H217-H223 ◽  
Author(s):  
Terese M. Zidon ◽  
Don D. Sheriff
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Important Determinant ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Ventricular Pacing ◽  
Autonomic Blockade ◽  
Distribution Of Cardiac Output

The distribution of cardiac output between compliant vasculature (e.g., splanchnic organs and skin) and noncompliant vasculature (e.g., skeletal muscle) is proposed to constitute an important determinant of the amount of blood available to the heart (central blood volume and pressure). The aim here was to directly test the hypothesis that diversion of blood flow from a relatively noncompliant vasculature (muscle) to compliant vasculature (splanchnic organs and skin) acts to reduce right atrial pressure. The approach was to inflate an occluder cuff on the terminal aorta for 30 s in one of two modes of ventricular pacing in five awake dogs with atrioventricular block and autonomic blockade. In one trial, cardiac output was maintained constant, meaning cuff inflation caused a portion of terminal aortic flow (a noncompliant circulation) to be diverted to the splanchnic and skin circulations (compliant circulations). In the other trial, arterial pressure was maintained constant, meaning blood flow to these other regions did not change. The response of right atrial pressure (corrected for differences in arterial pressure between the two trials) fit our hypothesis, being lower when blood flow was diverted to compliant regions. We conclude that a small (4% of cardiac output) diversion of blood flow from a noncompliant region to a compliant region reduces right atrial pressure by 0.7 mmHg.

Starling's "Law of the Heart": Rise and Fall of the Descending Limb

Physiology ◽  
1992 ◽  
Vol 7 (3) ◽  
pp. 134-137 ◽  
Author(s):  
Gijs Elzinga
Keyword(s):  
Cardiac Output ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Starling’S Law ◽  
Original Meaning ◽  
The Law

The descending limb of Starling's relationship between right atrial pressure and cardiac output was the cornerstone of his "law of the heart"; it was widely accepted in physiology. However, the original meaning of the law faded away over the years; the descending limb proved to be an experimental artefact.

Influence of the renal nerves on sodium excretion during progressive reductions in cardiac output

1995 ◽  
Vol 269 (3) ◽  
pp. R678-R690 ◽  
Author(s):  
T. E. Lohmeier ◽  
G. A. Reinhart ◽  
H. L. Mizelle ◽  
J. P. Montani ◽  
R. Hester ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Sodium Excretion ◽  
Pressure Control ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Renal Nerves ◽  
Sodium Retention

The purpose of this study was to elucidate the role of the renal nerves in promoting sodium retention during chronic reductions in cardiac output. In five dogs, the left kidney was denervated and the urinary bladder was surgically divided to allow separate 24-h urine collection from the innervated and denervated kidneys. Additionally, progressive reductions in cardiac output were achieved by employing an externally adjustable occluder around the pulmonary artery and by servo-controlling right atrial pressure (control = 0.9 +/- 0.2 mmHg) at 4.7 +/- 0.1, 7.5 +/- 0.1, and 9.8 +/- 0.2 mmHg for 3 days at each level. At the highest level of right atrial pressure, the 24-h values for mean arterial pressure (control = 97 +/- 3 mmHg) and cardiac output (control = 2,434 +/- 177 ml/min) were reduced approximately 25 and 55%, respectively; glomerular filtration rate fell by approximately 35% and renal plasma flow by approximately 65%. However, despite the sodium retention induced by these hemodynamic changes, there were no significant differences in renal hemodynamics or sodium excretion between the two kidneys during pulmonary artery constriction. In contrast, after release of the pulmonary artery occluder on day 9, sodium excretion increased more (approximately 28% during the initial 24 h) in innervated than in denervated kidneys. These results suggest that the renal nerves are relatively unimportant in promoting sodium retention in this model of low cardiac output but contribute significantly to the short-term elimination of sodium after partial restoration of cardiac output and mean arterial pressure.

Mechanism of decrease in cardiac output caused by opening the chest

1964 ◽  
Vol 207 (5) ◽  
pp. 1112-1116 ◽  
Author(s):  
Jose D. Fermoso ◽  
Travis Q. Richardson ◽  
Arthur C. Guyton
Keyword(s):  
Cardiac Output ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Cardiopulmonary Function ◽  
Lower Cardiac Output

The cardiac output in ten dogs fell an average of 18.8% (±1.1 sem) when the chest was opened. Opening the chest, which increased the extracardiac pressure, shifted the cardiopulmonary-function curve (relating right atrial pressure to cardiac output) toward higher atrial pressure levels. This caused the cardiopulmonary curve to equate with the animal's systemic-function curve at a lower cardiac output; the greater the extracardiac pressure the lower the output. Thus, changes in extracardiac pressure can alter cardiac output even though the pumping ability of the heart is not altered.

Control of right atrial pressure at constant cardiac output suppresses volume natriuresis in anesthetized rats

1984 ◽  
Vol 62 (7) ◽  
pp. 798-801 ◽  
Author(s):  
U. Ackermann ◽  
J. R. Rudolph
Keyword(s):  
Blood Volume ◽  
Volume Expansion ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Control Value ◽  
Volume Load ◽  
Arterial Blood ◽  
Anesthetized Rats ◽  
Blood Volume Expansion

The blood volume of anesthetized rats was expanded acutely by 33% with donor blood while a caval snare was gradually tightened so that right atrial pressure (RAP) was prevented from rising (n = 6). In control experiments (n = 5) an aortic snare was used to hold mean arterial blood pressure near the values found in the experimental series. However, RAP was allowed to change freely and increased by 1.6 ± 0.4 mmHg (1 mmHg = 133.322 Pa) during volume expansion. When the two groups were compared, there were no significant differences between their mean arterial blood pressures (near 110 mmHg) or in their cardiac outputs (near 0.25 mL∙min−1∙g body weight−1). There were, however, significant differences between their renal responses to the volume load. When RAP was free to change, the rate of volume excretion [Formula: see text] increased to 30 ± 15 (SEM) μL∙min−1∙g kidney weight−1 (KW) from its control value of 3.49 ± 0.31 and the rate of sodium excretion [Formula: see text] increased to 3.59 ± 0.20 μequiv.∙min−1∙g KW−1 from its preinfusion value of 0.42 ± 0.10. When RAP was not allowed to increase during volume loading, [Formula: see text] and [Formula: see text] did not change from their respective preinfusion values (2.99 ± 0.46 μL∙min−1∙g KW−1 and 0.35 ± 0.10 μequiv.∙min−1∙g KW−1). The results imply that during acute blood volume expansion increased central vascular pressure is a prerequisite for the homeostasis of body water and salt.

scholarly journals Effect of Exercise on Cerebral Circulation

1983 ◽  
Vol 3 (3) ◽  
pp. 287-290 ◽  
Author(s):  
Mordecai Globus ◽  
Eldad Melamed ◽  
Andre Keren ◽  
Dan Tzivoni ◽  
Chaim Granot ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Physical Exercise ◽  
Normal Subjects ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Inhalation Technique ◽  
Cerebrovascular Autoregulation ◽  
Cerebrovascular Resistance

The effect of supine physical exercise on cerebral blood flow (CBF) was measured in 30 normal subjects with the 133Xe inhalation technique. The CBF measurements were correlated to changes in Pco2, heart rate, and blood pressure, and to cardiac output and right atrial pressure in 10 of the subjects who underwent Swan-Ganz catheterization. No significant change was found in CBF during physical exercise, although a marked increase in cardiac output, blood pressure, and right atrial pressure and a mild decrease in PCO2 were found. Cerebrovascular resistance increased by 38%, in contrast to a decrease of 33% in the peripheral vascular resistance. The factors that affect the mechanism of cerebrovascular autoregulation during exercise are discussed.

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