The role of cardiac receptor and arterial baroreceptor reflexes in control of the circulation during acute change of blood volume in the conscious rabbit.

Ludbrook, John; Graham, William F.

doi:10.1161/01.res.54.4.424

Cited by 63 publications

(46 citation statements)

References 41 publications

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“…The gradual rise in venous compliance during the exposure to an increased volume is paralleled by a gradual fall in venous pressure and, with it, normalization of the initially elevated venous return. The immediate 5% rise in MAP after rapid volume loading can be expected to contribute to the normalization of the acutely elevated CO through activation of the baroreceptor, a mechanism supported by previous studies (22).…”

Section: Discussionsupporting

confidence: 68%

Hemodynamic Response to Volume Stress in Awake Late-Pregnant and Nonpregnant Rats

et al. 1991

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Section: Discussionsupporting

confidence: 68%

Hemodynamic Response to Volume Stress in Awake Late-Pregnant and Nonpregnant Rats

et al. 1991

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“…The initial compensatory vasoconstriction is reflex in origin and is due principally to unloading of the arterial baroreceptors (Ludbrook & Graham, 1984). There is strong evidence that its subsequent failure is triggered by a signal from the heart (Burke & Dorward, 1988;Evans et al, 1989a).…”

Section: Introductionmentioning

confidence: 99%

Effects of μ‐opioid receptor agonists on circulatory responses to simulated haemorrhage in conscious rabbits

Evans

Ludbrook

1990

British J Pharmacology

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1 Cardiac output, arterial pressure, heart rate, systemic vascular conductance, respiratory rate and arterial blood Po2 and Pco2 were measured in unanaesthetized rabbits. Haemorrhage was simulated by inflating a cuff placed around the inferior vena cava so that cardiac output fell at a constant rate of about 8% of its resting value per min. 2 The effects of drug treatments on resting haemodynamic and respiratory variables, and on the haemodynamic response to simulated haemorrhage, were tested. The treatments were; 4th ventricular (-)-naloxone HCl (10-100 nmol), 4th ventricular H-Tyr-D-Ala-Gly-MePhe-NH(CH2)20H (DAMGO; 30-300pmol), and i.v. morphine sulphate (0.5-5.Opmolkg1'). The interactions of graded 4th ventricular doses of naloxone (3-100nmol) with the actions of DAMGO (100-300pmol) on these responses were also assessed. 3 After sham treatments, the circulatory response to simulated haemorrhage had two phases. During the first compensatory phase, systemic vascular conductance fell, heart rate rose, and mean arterial pressure fell by only about 7mmHg. A second decompensatory phase supervened when cardiac output had fallen by about 50%. At this point systemic vascular conductance rose abruptly and arterial pressure fell to <40mmHg. 4 Low 4th ventricular doses of naloxone (10-30nmol) and DAMGO (30-l00pmol) had no discernible effect on the circulatory response to simulated haemorrhage. Higher doses of naloxone (30-100 nmol) and DAMGO (100-300pmol) prevented the decompensatory phase. These high doses of naloxone and DAMGO lowered resting heart rate without affecting the other haemodynamic or respiratory variables.5 Low doses of i.v. morphine (0.5-1.Spumolkg-1) also had no discernible effect on the circulatory response to simulated haemorrhage. Higher doses of morphine (1.5-5.Opmol kg 1) abolished the decompensatory phase. These high doses caused respiratory depression without affecting the resting haemodynamic variables. 6 The prevention of circulatory decompensation by high doses of DAMGO was reversed by 3-10nmol of naloxone in 3 out of 4 rabbits and by 10-30 nmol of naloxone in all 4 rabbits. The decompensatory phase was, however, prevented by the combined high doses of DAMGO (100-300pmol) and naloxone (30-100 nmol). 7 These findings provide strong evidence that activation of u-opioid receptors in the central nervous system abolishes circulatory decompensation during acute reduction of central blood volume in conscious rabbits. This effect does not appear to be due to activation of arterial chemoreceptors or to a non-specific increase in sympathetic vasoconstrictor drive, since respiratory depression and hypertension were not observed after 4th ventricular doses of DAMGO which abolished circulatory decompensation. Our results also provide indirect confirmation of our previous finding that naloxone acts to prevent circulatory decompensation by an antagonist action at central 6-receptors.

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“…Initially, systemic vascular resistance rises as blood volume and cardiac output fall, so that arterial pressure is well maintained (Schadt, McKown, McKown & Franklin, 1984;Ludbrook & Rutter, 1988). This compensatory vasoconstriction is chiefly attributable to the action of the arterial baroreceptor reflex (Ludbrook & Graham, 1984;Schadt & Gaddis, 1986). But if acute blood loss exceeds 30 % of blood volume the compensatory vasoconstriction fails and blood pressure falls abruptly (Schadt et al 1984;Ludbrook & Rutter, 1988).…”

Section: Introductionmentioning

confidence: 99%

Role of central opiate receptor subtypes in the circulatory responses of awake rabbits to graded caval occlusions.

Evans

Ludbrook

Leeuwen

1989

The Journal of Physiology

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SUMMARY1. In unanaesthetized rabbits, haemorrhage was simulated by inflating a cuff placed round the inferior vena cava so that cardiac output fell at a constant rate of 8 % of its resting value per minute. The circulatory responses were measured after injections into the fourth ventricle of saline vehicle, selective opioid antagonists, selective opioid agonists, and agonist-antagonist mixtures. Three sets of experiments were done to determine if a specific subtype of opiate receptor within the central nervous system is responsible for the circulatory decompensation that occurs during simulated haemorrhage.2. In six rabbits the effects of ascending doses of the antagonists naloxone (,uZselective), Mr 2266 (K-and ,t-selective), ICI 174864 (6-selective) and nor-binaltorphimine (K-selective) were tested. In three rabbits the effects of the antagonist naloxone, the agonists HTyr-D-Ala-Gly-MePhe-NH(CHi)2OH (DAGO, ,u-selective), U 50488H (K-selective), and [D-Pen2, D-Pen5]-enkephalin (DPDPE, 6-selective), and combinations of these agonists with naloxone were tested. In four rabbits the doserelated effects of DAGO on respiratory, as well as circulatory, functions were examined.3. After injecting saline vehicle, the circulatory response to simulated haemorrhage had two phases. During the first phase, systemic vascular conductance fell, heart rate rose, and mean arterial pressure fell by only -10 mmHg. A second, decompensatory, phase began when cardiac output had fallen to -50 % of its resting level. At this point, there was an abrupt rise in systemic vascular conductance and a fall in mean arterial pressure to < 40 mmHg.4. The lower range of doses of naloxone (3-30 nmol), Mr 2266 (10-100 nmol), ICI 174864 (10-30 nmol), and all doses of nor-binaltorphimine (1-100 nmol), were without effect on the circulatory response to simulated haemorrhage. Higher doses of naloxone (30-100 nmol), Mr 2266 (100-300 nmol) and ICI 174864 (30-100 nmol) abolished the decompensatory phase. The relative order of antagonist potency was ICI 174864 > naloxone > Mr 2266 > nor-binaltorphimine.5. In the second set of experiments, the critical dose of naloxone necessary to prevent circulatory decompensation during simulated haemorrhage was 30-150 1.S 74: 16 R. G. EVANS, J. LUDBROOK AND A. F. VANLEEUWEN nmol. The d-agonist DPDPE (50 nmol) did not affect the haemodynamic response to simulated haemorrhage, but it did block the effect of naloxone on the response. The u-agonist DAGO (30 nmol) and the K-agonist U 50488H (300 nmol) prevented circulatory decompensation during simulated haemorrhage, whether given alone or in combination with the critical dose of naloxone, but DAGO (30 mmol) also raised arterial pressure, lowered systemic vascular conductance and slowed respiration.6. In the third set of experiments we found that lower doses of DAGO (100-300 pmol) would also prevent circulatory decompensation during simulated haemorrhage. These doses did not affect resting arterial pressure or systemic vascular conductance, and had insignificant effects on res...

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The role of cardiac receptor and arterial baroreceptor reflexes in control of the circulation during acute change of blood volume in the conscious rabbit.

Cited by 63 publications

References 41 publications

Hemodynamic Response to Volume Stress in Awake Late-Pregnant and Nonpregnant Rats

Hemodynamic Response to Volume Stress in Awake Late-Pregnant and Nonpregnant Rats

Effects of μ‐opioid receptor agonists on circulatory responses to simulated haemorrhage in conscious rabbits

Role of central opiate receptor subtypes in the circulatory responses of awake rabbits to graded caval occlusions.

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