Control of cardiac output by regional blood flow distribution

Coleman, Thomas G.; ManningJr., R. Davis; NormanJr., Roger A.; Guyton, Arthur C.

doi:10.1007/bf02368487

Cited by 41 publications

(35 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Any changes induced by TPR changes can be excluded also, since TPR changes appear to be secondary to MABP fluctuations rather than casual. This conclusion is at variance with the idea that CO is determined primarily by the sum of peripheral tissue needs (Coleman et al, 1974).…”

Section: Figure 6 Average Cross-spectra Between Mean Arterial Blood Pmentioning

confidence: 75%

Oscillations in mean arterial blood pressure in conscious dogs.

Shimada¹,

Marsh²

1979

Circulation Research

View full text Add to dashboard Cite

SUMMARY Oscillations in mean arterial blood pressure (MABP) with periods near 1.5 hours were observed in conscious male dogs with pressure transducers implanted in their aortas. Cardiac output (CO) was measured with an electromagnetic flow probe implanted about the ascending aorta, and total peripheral resistance (TPR) was calculated as the ratio of MABP to CO. Heart rate (HR) was measured with a cardiotachometer. Coherence functions were calculated among the four variables (MABP, TPR, CO, and HR) to determine significant oscillations at the frequency of the MABP oscillation. Crossspectral calculations produced phase relationships among the variables. TPR and CO were both oscillating at the same frequency as MABP. However, TPR lagged MABP by 63 degrees, whereas the phase angle for CO and MABP was not significantly different from zero. We concluded that CO must be producing the MABP oscillations, and that the TPR oscillations arose as a reaction to the MABP or CO changes. HR was oscillating in phase with CO, indicating that CO fluctuations were induced in part by HR changes and that the sympathetic nervous system was probably driving the heart. In further experiments, chronic dietary sodium changes did not alter the power spectra for MABP. Thus, the renin-angiotensin system (RAS) was not responsible for the oscillations; conversely, the oscillations were not acting as a signal to the RAS during sodium-deficient states, a condition known to stimulate the RAS. Circ Res 44; 692-700, 1979 CARDIOVASCULAR periodicities have been known since man first felt his pulse, but the heart beat and circadian rhythms are the only frequencies that have attracted much attention. Rhythms lying between these two extremes have been reported for a number of physiological variables (Kleitman, 1963;Krieger et al., 1971;Lenfant, 1967;Ookhtens et al., 1974;Yamaji et al., 1972), but not for the circulation. We speculated, from very general considerations, that flows and pressures might fluctuate periodically at an intermediate frequency (Marsh, 1973), and the major purpose of this paper is to report observations of such oscillations in mean arterial blood pressure (MABP), cardiac output (CO), heart rate (HR), and total peripheral resistance (TPR) in conscious dogs. The period length is 1.5 hours.An important unresolved question in the area of fluid volume regulation is the identification of the signal that triggers reiim release when extracellular fluid volume is depleted, as during dietary NaCl restriction. Arterial blood pressure governs renin release, at least in part, but MABP remains normal over a wide range of renin secretion rates (Davis and Freeman, 1976). We therefore speculated that a blood pressure signal that varied in the frequency domain, rather than in the amplitude domain, might cause the change in renin release when extracellular fluid volume varies (Marsh, 1973). We have tested this hypothesis by examining the effect of dietary NaCl restriction on the MABP oscillations.Methods Male mongrel dogs weighing 22-32 kg were di...

show abstract

Section: Figure 6 Average Cross-spectra Between Mean Arterial Blood Pmentioning

confidence: 75%

Oscillations in mean arterial blood pressure in conscious dogs.

Shimada¹,

Marsh²

1979

Circulation Research

View full text Add to dashboard Cite

show abstract

“…Experimentally, cardiac output can be increased by mechanical obstruction of the descending aorta (Barcroft & Samaan, 1935) or of the superior mesenteric artery (Groszmann, Blei, Kniaz, Storer & Conn, 1978). Theoretical models (Coleman et al 1973;Caldini et al 1974) show the basis of the blood displacement to be diversion of flow by differential arterial constriction from a vascular bed with a long time constant for venous drainage to a parallel bed with a short time constant.…”

Section: Displacement Of Blood From the Splanchnic Vasculaturementioning

confidence: 99%

“…were increased by expansion of the circulating blood volume. An alternative physiological mechanism may be an increase of activity in the splanchnic vasoconstrictor nerves, which would displace blood from the large portal, hepatic and splenic capacitances by active contraction of their walls (Mellander, 1960;Karim & Hainsworth, 1976; Rothe, 1983) and by passive drainage consequent upon a reduced arterial inflow (Krogh, 1912;Barcroft & Samaan, 1935; Coleman, Manning, Norman & Guyton, 1973;Caldini, Permutt, Waddell & Riley, 1974). Tigerstedt (1909) first observed that stimulation of the peripheral end of the splanchnic nerve in the rabbit could increase pressure and blood flow in the aorta despite a fall in heart rate.…”

mentioning

confidence: 99%

Haemodynamic responses to stimulation of the splanchnic and cardiac sympathetic nerves in the anaesthetized cat.

Barnes¹,

Bower²,

Rink³

1986

The Journal of Physiology

View full text Add to dashboard Cite

SUMMARY1. The changes in cardiac output and mean right atrial pressure (R.A.P.) evoked at different circulating blood volumes by stimulation of the splanchnic sympathetic nerves were investigated in adrenalectomized cats under chloralose anaesthesia, with unopened chests and spontaneous respiration and with active vascular reflexes. The cardiac autonomic nerves were cut or blocked pharmacologically.2. Stimulation of the distal ends of the splanchnic nerves at 4 Hz caused aortic pressure and R.A.P. to rise to maximum values at 2 min before declining slowly. Cardiac output rose more slowly to a steady state at 3 min; at higher circulating volumes it fell initially. Although the output increments were slower in development they were better sustained than those in total peripheral resistance. The proportionate output increments were largest and the R.A.P. increments least at low circulating volumes whereas at high volumes the R.A.P. increments were large but the output changes were small or negative; the pattern of changes resembled that resulting from infusion of blood.3. Stimulation of the cardiac sympathetic nerves evoked a rise in output and a fall in R.A.P. related in magnitude to the initial value of R.A.P. On simultaneous stimulation of the splanchnic and cardiac sympathetic nerves the changes in output combined whereas the R.A.P. changes cancelled, to give output increments of 25-50 % with little change in R.A.P. at all circulating volumes.4. At high circulating volumes infusion of blood did not usually alter output or aortic pressure, but splanchnic nerve stimulation increased peripheral resistance and aortic pressure and commonly evoked a rise in left ventricular stroke work which could not be accounted for by known adrenergic mechanisms or by elevation of left ventricular end-diastolic pressure.5. Portal venous pressure was consistently elevated by splanchnic nerve stimulation; it rose more slowly than did aortic pressure or R.A.P. and was independent of a changing central venous pressure provided this did not exceed +5 mmHg. The cardiac output increments were not related to changes in the ratio between the input

show abstract

“…The amount of blood which can be mobilized from the entire systemic vascular bed by the reflex has also been quantified (Drees and Rothe, 1974;Rashkind et al, 1953;Shoukas and Sagawa, 1973). However, the exact mechanism and source of blood mobilization remains somewhat controversial (Caldini et al, 1974;Coleman et al, 1974;Green, 1975;Mitzner and Goldberg, 1975).Using a dog preparation in which venous return was diverted into a reservoir while cardiac output was kept constant, Shoukas and Sagawa (1973) showed that significant shifts of blood between the dog and a reservoir occurred when carotid sinus pressure was changed. They hypothesized that the reflex altered the "unstressed" vascular volume of the systemic veins based on the finding that the total systemic vascular compliance did not change significantly.…”

mentioning

confidence: 99%

mentioning

confidence: 99%

The effect of the carotid sinus baroreceptor reflex on blood flow and volume redistribution in the total systemic vascular bed of the dog.

Brunner¹,

Shoukas²,

MacAnespie³

1981

Circulation Research

View full text Add to dashboard Cite

SUMMARY To quantify the relative contribution of blood flow redistribution and active changes in vascular capacity in the regulation of cardiac output, blood flow and volumes in two parallel vascular beds were measured in response to varying carotid sinus pressures. In nine dogs, carotid sinuses were isolated and intrasinus pressure was controlled. Two external reservoirs were placed between the caval veins and the right heart to measure changes in vascular capacity in splanchnic and extrasplanchnic vascular beds. At intrasinus pressures of SO and 200 nun Hg, we have simultaneously measured arterial resistances, compliances, changes in flows, and "unstressed vascular volume," and time constants of venous drainage in the splanchnic and extrasplanchnic vascular beds. Compliances and time constants of venous drainage were found to be nearly equal in the two beds. A decrease in intrasinus pressure from 200 to 50 mm Hg resulted in a small redistribution of blood flow (about 5% of cardiac output) from the extraplanchnic compartment to the splanchnic vascular bed. Changes in reservoir volumes were found to be around 7.0 ml/kg. The splanchnic vascular bed was responsible for a greater change in reservoir volume for a given change in intrasinus pressure. With any change in intrasinus pressure, the change in arterial resistance in the extrasplanchnic vascular bed was greater than that of the splanchnic vascular bed. Blood flow redistribution was not found to be a significant factor contributing to changes in reservoir volume. The changes in reservoir volume seen, must have been due to active changes in vascular capacity in the two channels chosen. Circ Res 48: 274-285, 1981 THE importance of changes in the capacitive property of the systemic vascular bed has been recognized for some time. For example, a decrease in capacity can increase the filling presure of the right heart which, in turn, can increase cardiac output. Evidence that the carotid sinus baroreceptor reflex controls the systemic vascular capacity has been presented from several laboratories (Drees and Rothe, 1974;Rashkind et al., 1953;Salzman, 1957;Shoukas and Sagawa 1973). The amount of blood which can be mobilized from the entire systemic vascular bed by the reflex has also been quantified (Drees and Rothe, 1974;Rashkind et al., 1953;Shoukas and Sagawa, 1973). However, the exact mechanism and source of blood mobilization remains somewhat controversial (Caldini et al., 1974;Coleman et al., 1974;Green, 1975;Mitzner and Goldberg, 1975).Using a dog preparation in which venous return was diverted into a reservoir while cardiac output was kept constant, Shoukas and Sagawa (1973) showed that significant shifts of blood between the dog and a reservoir occurred when carotid sinus pressure was changed. They hypothesized that the reflex altered the "unstressed" vascular volume of the systemic veins based on the finding that the total systemic vascular compliance did not change significantly. A more recent work by Shoukas and Brunner (1980) indicated that the reflex...

show abstract

Control of cardiac output by regional blood flow distribution

Cited by 41 publications

References 23 publications

Oscillations in mean arterial blood pressure in conscious dogs.

Oscillations in mean arterial blood pressure in conscious dogs.

Haemodynamic responses to stimulation of the splanchnic and cardiac sympathetic nerves in the anaesthetized cat.

The effect of the carotid sinus baroreceptor reflex on blood flow and volume redistribution in the total systemic vascular bed of the dog.

Contact Info

Product

Resources

About