The circulatory effects of acute hypervolemia and hemodilution in conscious rabbits.

Faris, Irwin; Iannos, J.; Jamieson, Glyn G.; Ludbrook, John

doi:10.1161/01.res.48.6.825

Cited by 27 publications

(15 citation statements)

References 29 publications

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“…Blood loss was 1 I .7 f 3.8 mL. This was replaced by low molecular weight dextran (Rheomacrodex, Pharmacia), diluted with saline so that it was isosmolar with plasma (Faris et al 1981). The rabbit was then paralysed with intravenous vecuronium (100 pg/kg followed by 5 pg/ kg per min) and artificially ventilated with 100% 0 2 at 1 L/min.…”

Section: Interruption Of Vagal Conductionmentioning

confidence: 99%

CHARACTERISTICS OF CARDIOVASCULAR REFLEXES ORIGINATING FROM 5‐HT₃ RECEPTORS IN THE HEART AND LUNGS OF UNANAESTHETIZED RABBITS

Evans

Ludbrook

Michalicek

1990

Clin Exp Pharma Physio

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1. When phenylbiguanide (1-PBG) (6.25-400 micrograms) was injected into the left atrium, right atrium or pulmonary artery of unanesthetized rabbits it caused dose-dependent falls of heart rate and arterial pressure, and short-lived hypopnoea or apnoea. The threshold dose was 50-100 micrograms. Maximal falls of heart rate (86-108 beats/min) and arterial pressure (33-35 mmHg) occurred at a dose of 200 micrograms. The latency between injection and onset of the bradycardia was 2.2-2.6 s and did not depend on the route. Cardiac output fell transiently with heart rate, but at the time of the maximal fall of arterial pressure it had returned to normal. All effects were abolished by intrapericardial procaine. The haemodynamic effects were exaggerated by sino-aortic barodenervation. Intrapericardial 1-PBG (200-400 micrograms) was without effect. Injection of 1-PBG (greater than 50-100 micrograms) into the aortic arch caused a variable increase in heart rate and arterial pressure. 2. When both cervical vagus nerves were crushed the depressor effects of atrial 1-PBG were reduced by only 76-84%. 3. The dose-response curves for left atrial and pulmonary artery injection of 1-PBG were shifted successively to the right by intravenous infusion of the 5-HT3 antagonist MDL72222 (0.1 and 1.0 mg/kg). 4. We conclude that in unanesthetized rabbits left atrial 1-PBG selectively excites myocardial afferents, whereas right atrial or pulmonary artery 1-PBG excites afferents that originate close to the pulmonary vasculature. In each case 1-PBG acts through pharmacologically specific 5-HT3 receptors. The afferents run mainly, but not exclusively, in the vagus nerves. The reflex fall of arterial pressure is accounted for almost entirely by a decrease in peripheral resistance.

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Section: Interruption Of Vagal Conductionmentioning

confidence: 99%

CHARACTERISTICS OF CARDIOVASCULAR REFLEXES ORIGINATING FROM 5‐HT₃ RECEPTORS IN THE HEART AND LUNGS OF UNANAESTHETIZED RABBITS

Evans

Ludbrook

Michalicek

1990

Clin Exp Pharma Physio

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“…Two to three weeks later an electromagnetic flow probe (Biotronex BL5050) was placed around the ascending aorta. The flow probes had previously been calibrated in vitro by use of cellophane dialysis tubing and human whole blood with a haematocrit of 38% (Faris et al, 1981). Two weeks later a polyvinyl chloride tube (Dural Plastics SV1O), which had been heated and drawn out, was introduced through the atlantooccipital ligament so that its 0.3mm o.d.…”

Section: Surgical Preparationmentioning

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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“…The first experiment was performed 7-10 days later, and next day a final operation was performed at which the carotid sinuses were denervated and both aortic nerves divided (Faris et al, 1981a). The second experiment was performed after a further 7-8 days.…”

Section: Surgical Proceduresmentioning

confidence: 99%

“…Donor blood was used for volume expansion, to avoid the confounding effects of hemodilution (Faris et al, 1981a). On the day before the experiment, the blood volume and hematocrit of the experimental rabbit were determined, and its blood cross-matched against that of a donor rabbit (Faris et al, 1981a).…”

Section: Preparations For the Experimentsmentioning

confidence: 99%

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

Ludbrook¹,

Graham²

1984

Circulation Research

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We have studied overall reflex control of the circulation by the arterial baroreceptors and cardiac receptors during acute change of blood volume in seven conscious rabbits. A factorial experimental design allowed analysis of the direction, magnitude, and significance of the reflex effects of independent input from each set of receptors, and the reflex interactions when the inputs were combined. Right atrial pressure, arterial pressure, systemic vascular resistance, cardiac output, and heart rate were measured during acute, graded, isohemic change of blood volume over the range +/- 27%. This was done with both reflexes present, only the arterial baroreceptor reflex present (intrapericardial 2% procaine), only the cardiac receptor reflex present (surgical baroreceptor denervation), and with both reflexes absent. As blood volume was depleted, the arterial baroreceptor reflex independently increased systemic vascular resistance and sustained arterial pressure, but the cardiac receptor reflex had no significant independent or interactive effects. As blood volume was expanded, each reflex had an independent effect in decreasing systemic vascular resistance and preventing arterial pressure from rising, the cardiac receptor reflex being the more powerful. Their effect in combination on systemic vascular resistance and arterial pressure was only two-fifths of the sum of their independent effects, so that they interacted negatively. In combination, the reflexes supported right atrial pressure during blood loss, despite their negative interaction, but did not significantly affect the relation of cardiac output to blood volume change in either direction. Thus both reflexes have important actions in moderating the overall effects of acute blood volume changes in conscious rabbits, but these are markedly diminished by their interactions.

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The circulatory effects of acute hypervolemia and hemodilution in conscious rabbits.

Cited by 27 publications

References 29 publications

CHARACTERISTICS OF CARDIOVASCULAR REFLEXES ORIGINATING FROM 5‐HT₃ RECEPTORS IN THE HEART AND LUNGS OF UNANAESTHETIZED RABBITS

CHARACTERISTICS OF CARDIOVASCULAR REFLEXES ORIGINATING FROM 5‐HT₃ RECEPTORS IN THE HEART AND LUNGS OF UNANAESTHETIZED RABBITS

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

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

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The circulatory effects of acute hypervolemia and hemodilution in conscious rabbits.

Cited by 27 publications

References 29 publications

CHARACTERISTICS OF CARDIOVASCULAR REFLEXES ORIGINATING FROM 5‐HT3 RECEPTORS IN THE HEART AND LUNGS OF UNANAESTHETIZED RABBITS

CHARACTERISTICS OF CARDIOVASCULAR REFLEXES ORIGINATING FROM 5‐HT3 RECEPTORS IN THE HEART AND LUNGS OF UNANAESTHETIZED RABBITS

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

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

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Product

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CHARACTERISTICS OF CARDIOVASCULAR REFLEXES ORIGINATING FROM 5‐HT₃ RECEPTORS IN THE HEART AND LUNGS OF UNANAESTHETIZED RABBITS

CHARACTERISTICS OF CARDIOVASCULAR REFLEXES ORIGINATING FROM 5‐HT₃ RECEPTORS IN THE HEART AND LUNGS OF UNANAESTHETIZED RABBITS