Vascular capacitance and cardiac output in pacing-induced canine models of acute and chronic heart failure

1995 ◽  
Vol 73 (11) ◽  
pp. 1641-1650 ◽  
Author(s):  
Richard Ian Ogilvie ◽  
Danuta Zborowska-Sluis
Keyword(s):  
Heart Failure ◽  
Cardiac Output ◽  
Chronic Heart Failure ◽  
Blood Volume ◽  
Central Blood Volume ◽  
Ventricular Pacing ◽  
Volume Loading ◽  
Total Blood ◽  
Volume Load ◽  
Vascular Capacitance

The relationship between stressed and total blood volume, total vascular capacitance, central blood volume, cardiac output (CO), and pulmonary capillary wedge pressure (Ppcw) was investigated in pacing-induced acute and chronic heart failure. Acute heart failure was induced in anesthetized splenectomized dogs by a volume load (20 mL/kg over 10 min) during rapid right ventricular pacing at 250 beats/min (RRVP) for 60 min. Chronic heart failure was induced by continuous RRVP for 2–6 weeks (average 24 ± 2 days). Total vascular compliance and capacitance were calculated from the mean circulatory filling pressure (Pmcf) during transient circulatory arrest after acetylcholine at three different circulating volumes. Stressed blood volume was calculated as a product of compliance and Pmcf, with the total blood volume measured by a dye dilution. Central blood volume (CBV) and CO were measured by thermodilution. Central (heart and lung) vascular capacitance was estimated from the plot of Ppcw against CBV. Acute volume loading without RRVP increased capacitance and CO, whereas after volume loading with RRVP, capacitance and CO were unaltered from baseline. Chronic RRVP reduced capacitance and CO. All interventions, volume ± RRVP or chronic RRVP, increased stressed and central blood volumes and Ppcw. Acute or chronic RRVP reduced central vascular capacitance. Cardiac output was increased when stressed and unstressed blood volumes increased proportionately as during volume loading alone. When CO was reduced and Ppcw increased, as during chronic RRVP or acute RRVP plus a volume load, stressed blood volume was increased and unstressed blood volume was decreased. Thus, interventions that reduced CO and increased Ppcw also increased stressed and reduced unstressed blood volume and total vascular capacitance.Key words: vascular capacitance, vascular compliance, central blood volume, rapid ventricular pacing, dogs, heart failure.

Circulation of sympathectomized dogs under pentobarbital anesthesia

1965 ◽  
Vol 208 (4) ◽  
pp. 790-794
Author(s):  
Shu Chien ◽  
Shunichi Usami
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Blood Volume ◽  
Total Blood Volume ◽  
Central Blood Volume ◽  
Total Blood ◽  
Pentobarbital Anesthesia ◽  
Blood Flows ◽  
The Mean ◽  
Mean Circulation

In sympathectomized-splenectomized dogs under pentobarbital anesthesia, the total blood volume averaged 78 ml/kg, with 20% in the splanchnic circulation and 28% in the central blood volume. These values are almost the same as those found in the splenectomized (control) dogs with the sympathetic system intact. The over-all and the splanchnic Fcells factors are also not significantly different between these two groups. The sympathectomized animals had lower arterial pressure, cardiac output, and splanchnic blood flow, but the resistances calculated for the total and the splanchnic circulations were not significantly different from those of the control dogs. The mean circulation times for the total, the central, and the splanchnic circulations were all longer in the sympathectomized dogs. The data indicate that, under pentobarbital anesthesia, sympathectomized dogs are characterized by slower blood flows without any significant changes in either the blood volume or vascular resistance.

Effect of experimental heart failure on peripheral sympathetic vasoconstriction

1988 ◽  
Vol 254 (4) ◽  
pp. H727-H733 ◽  
Author(s):  
J. R. Wilson ◽  
W. Matthai ◽  
V. Lanoce ◽  
M. Frey ◽  
N. Ferraro
Keyword(s):  
Heart Failure ◽  
Cardiac Output ◽  
Chronic Heart Failure ◽  
Neurotransmitter Release ◽  
Ventricular Pacing ◽  
Low Cardiac Output ◽  
Vascular Responses ◽  
Experimental Heart Failure ◽  
Sympathetic Vasoconstriction ◽  
Rapid Ventricular Pacing

To investigate whether heart failure impairs peripheral sympathetic vasoconstriction, hindlimb vascular responses to lumbar chain stimulation (0.5-20 Hz) were studied in normal dogs and in dogs with chronic heart failure produced by rapid ventricular pacing. At lumbar chain stimulation rates of 0.5-3 Hz, hindlimb vascular responses were comparable in both groups. However, at stimulation rates of 5-20 Hz, vascular responses were significantly attenuated in the dogs with heart failure. Vascular responses to norepinephrine (0.1, 1, and 10 micrograms/min) were not altered. These findings suggest that chronic heart failure results in impaired sympathetic vasoconstriction, probably because of reduced neurotransmitter release. This abnormality may interfere with the capacity of the failing circulation to compensate for a low cardiac output and thereby intensify the severity of heart failure.

scholarly journals Muscle metaboreflex-induced central blood volume mobilization in heart failure

2019 ◽  
Vol 316 (5) ◽  
pp. H1047-H1052 ◽  
Author(s):  
Donal S. O’Leary ◽  
Danielle Senador ◽  
Robert A. Augustyniak
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Cardiac Output ◽  
Blood Volume ◽  
Systolic Heart Failure ◽  
Normal Subjects ◽  
Dynamic Exercise ◽  
Central Blood Volume ◽  
Ventricular Contractility ◽  
Muscle Metaboreflex

Underperfusion of active skeletal muscle causes metabolites to accumulate and stimulate group III and IV skeletal muscle afferents, which triggers a powerful pressor response termed the muscle metaboreflex. Muscle metaboreflex activation (MMA) during submaximal dynamic exercise in healthy individuals increases arterial pressure mainly via substantial increases in cardiac output (CO). The increases in CO occur via the combination of tachycardia and increased ventricular contractility. Importantly, MMA also elicits substantial central blood volume mobilization, which allows the ventricular responses to sustain the increases in CO. Otherwise preload would fall and the increases in CO could not be maintained. In subjects with systolic heart failure (HF), the ability to increase CO during exercise and MMA is markedly reduced, which has been attributed to impaired ventricular contractility. Whether the ability to maintain preload during MMA in HF is preserved is unknown. Using a conscious chronically instrumented canine model, we observed that MMA in HF is able to raise central blood volume similarly as in normal subjects. Therefore, the loss of the ability to raise CO during MMA in HF is not because of the loss of the ability to mobilize blood volume centrally. NEW & NOTEWORTHY In normal subjects during dynamic exercise muscle metaboreflex activation elicits large increases in cardiac output that occur via increases in heart rate, ventricular contractility, and, importantly, marked central blood volume mobilization that acts to maintain ventricular preload, thereby allowing the changes in cardiac function to maintain the increases in cardiac output. In subjects with heart failure, the ability to raise cardiac output during muscle metaboreflex activation is impaired. We investigated whether this is because of the inability to maintain ventricular preload. We found that this reflex is still able to elicit large increases in central blood volume, and therefore the limited ability to raise cardiac output likely stems from ventricular dysfunction and not the ability to maintain preload.

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.

Observations on Cardiac Output and ”Pulmonary Blood Volume” in Normal Man by External Recording of the Intracardiac Flow of 131I Labelled Albumin

1961 ◽  
Vol 1 (04) ◽  
pp. 353-379
Author(s):  
Jacques Lammerant ◽  
Norman Veall ◽  
Michel De Visscher
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Normal Subjects ◽  
Published Data ◽  
Total Blood Volume ◽  
Total Blood ◽  
Pulmonary Blood Volume ◽  
Intracardiac Flow ◽  
Normal Man ◽  
Mean Circulation

Summary1. The technique for the measurement of cardiac output by external recording of the intracardiac flow of 131I labelled human serum albumin has been extended to provide a measure of the mean circulation time from right to left heart and hence a new approach to the estimation of the pulmonary blood volume.2. Values for the basal cardiac output in normal subjects and its variations with age are in good agreement with the previously published data of other workers.3. The pulmonary blood volume in normal man in the basal state was found to be 28.2 ± 0.6% of the total blood volume.4. There was no correlation between cardiac output and pulmonary blood volume in a series of normal subjects in the basal state.5. The increase in cardiac output during digestion was associated with a decrease in pulmonary blood volume equal to 6.3 ± 1.2% of the total blood volume, that is, about 280 ml.6. The increase in cardiac output during exercise was associated with a decrease in pulmonary blood volume equal to 4.5 ± 1.0% of the total blood volume, that is, about 200 ml.7. The increase in cardiac output attributed to alarm is not associated with a decrease in pulmonary blood volume, the latter may in fact be increased.8. The total blood volume is advocated as a standard of reference for studies of this type in normal subjects in preference to body weight or surface area.9. The significance of these results and the validity of the method are discussed.

Characterization of baroreflex impairment in conscious dogs with pacing-induced heart failure

1993 ◽  
Vol 265 (5) ◽  
pp. R1132-R1140 ◽  
Author(s):  
N. B. Olivier ◽  
R. B. Stephenson
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Peripheral Resistance ◽  
Open Loop ◽  
Ventricular Pacing ◽  
Baroreflex Control ◽  
Rapid Ventricular Pacing ◽  
Reflex Control

Open-loop baroreflex responses were evaluated in eight conscious dogs before and during congestive heart failure to determine the effects of failure on baroreflex control of blood pressure, heart rate, cardiac output, and total peripheral resistance. Heart failure was induced by rapid ventricular pacing. Baroreflex function was determined by calculation of the range and gain of the open-loop stimulus-response relationships for the effect of carotid sinus pressure on blood pressure, heart rate, cardiac output, and total peripheral resistance. The range and gain of blood pressure responses were substantially reduced as early as 3 days after induction of heart failure (161 +/- 6 to 99 +/- 8 mmHg and -2.7 +/- 0.3 to -1.5 +/- 0.1, respectively) and remained depressed for the 21 days of heart failure. This depression in baroreflex control of blood pressure was associated with similar depressions in reflex range and gain for heart rate (125 +/- 9 to 78 +/- 11 beats/min and -2.05 +/- 0.2 to -1.16 +/- 0.2 beats/min, respectively) and cardiac output (1.74 +/- 0.2 to 0.46 +/- 0.2 l/min and -0.81 +/- 0.02 to -0.027 +/- 0.008 l/min, respectively). The group-averaged range and gain for reflex control of vascular resistance were not altered by heart failure. In three dogs, discontinuation of rapid ventricular pacing led to resolution of heart failure within 7 days and partial restoration of the range and gain of reflex control of blood pressure. We conclude that heart failure reversibly depresses baroreflex control of blood pressure principally through a concurrent reduction in reflex control of cardiac output, whereas reflex control of vascular resistance is not consistently affected.

Cardiac output, GFR, and renal excretion rates during maintained volume load in rats

1978 ◽  
Vol 235 (6) ◽  
pp. H670-H676 ◽  
Author(s):  
U. Ackermann
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Renal Excretion ◽  
Venous Pressure ◽  
Circulating Blood Volume ◽  
Reservoir Volume ◽  
Volume Load ◽  
Blood Volume Expansion ◽  
Highly Correlated ◽  
Excretion Rates

The correlation among cardiac output (CO), glomerular filtration rate (GFR), fractional tubular sodium rejection (TFRNa), and renal excretion rates of water and salt was investigated during ischemic blood volume expansion in rats. Initially circulating blood volume was equilibrated isovolemically with a reservoir volume of 6% albumin solution equal to one-third the estimated blood volume. Later the equilibrated reservoir contents were infused intravenously. CO was measured by thermodilution, GFR by inulin clearance. Significant linear correlations existed between GFR and the rates of urine flow (r = 0.90), sodium excretion (r = 0.75) and potassium excretion (r = 0.76) that prevailed 5--10 min after a given GFR change. The increased GFR was highly correlated with CO (r = 0.94), probably correlated with mean central venous pressure (r = 0.45), but not correlated with mean abdominal aortic blood pressure. The correlation between CO and time-delayed (5--10 min) TRFNa was also highly significant (r = 0.98). The saluresis appears to have been caused initially by increased tubular load and subsequently by decreased absolute tubular reabsorption.

Kinetics of oxygen uptake at onset of exercise related to cardiac output, but not to arteriovenous oxygen difference in patients with chronic heart failure

1999 ◽  
Vol 83 (11) ◽  
pp. 1573-1576 ◽  
Author(s):  
Akihiro Matsumoto ◽  
Haruki Itoh ◽  
Ikuo Yokoyama ◽  
Teruhiko Aoyagi ◽  
Seiryo Sugiura ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Output ◽  
Chronic Heart Failure ◽  
Oxygen Uptake ◽  
Kinetics Of ◽  
Oxygen Difference

scholarly journals Effect of volume loading on the Frank-Starling relation during reductions in central blood volume in heat-stressed humans

2010 ◽  
Vol 588 (17) ◽  
pp. 3333-3339 ◽  
Author(s):  
M. Bundgaard-Nielsen ◽  
T. E. Wilson ◽  
T. Seifert ◽  
N. H. Secher ◽  
C. G. Crandall
Keyword(s):  
Blood Volume ◽  
Central Blood Volume ◽  
Volume Loading
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