Effects of respiratory acidosis on circulatory response to isoproterenol

Schroeder, JS; Robison, S L; Miller, H C; Harrison, D C

doi:10.1152/ajplegacy.1970.218.2.448

Cited by 14 publications

(9 citation statements)

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“…Although the administration of the gas did not significantly lower heart rate during the infusion, once the administration of CO2 was discontinued, there was an immediate marked increase in heart rate in all subjects. Our findings in man are in agreement with previous results reported from this labora-tory19 but differ slightly from observations in animals made by Schroeder and associates 18 who observed only attenuation of the chronotropic effect of isoproterenol with 10 per cent CO 2 • We hyperventilated 2 of our subjects shortly after the isoproterenol and noticed a large increase in heart rate. It is possible that, whereas a respiratory acidosis causes an attenuation of effect, hyperventilation and respiratory alkalosis potentiate the effect of isoproterenol on the heart.…”

Section: Discussionsupporting

confidence: 91%

“…MacLean and associates,l1 studying patients with the clinical syndrome of "shock" who had poor tissue perfusion, commented that the drug appeared more effective in those patients who compensated for their concomitant metabolic acidosis by hyperventilation than in those who did not. It has recently been shown in animals by Schroeder and associates 18 and by Xanalatos and James 19 that marked attenuation of isoproterenol vasodilatation occurs during respiratory acidosis. Both groups of workers showed that the chronotropic effects of an isoproterenol infusion were largely abolished by the inhalation of 5 per cent CO 2 • The purpose of this investigation was to determine the effect of 5 per cent CO 2 on the heart rate, blood pressure, and peripheral blood flow after isoproterenol infusion in man.…”

Section: Departments Of Medicine and Pharmacology Royal Free Hospitamentioning

confidence: 97%

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The effect of five per cent carbon dioxide on the response of muscle blood flow to isoproterenol in man

Xanalatos¹,

MacDonell²,

Larbi³

et al. 1973

Clin Pharma and Therapeutics

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Heart rate, muscle blood flow, and blood pressure were measured in 10 subjects. The administration of 5 per cent CO2 caused a fall in blood flow and an increase in mean arterial pressure without significant change in heart rate. An infusion of isoproterenol at a dose of 2 ug per minute caused an increase in flow, heart rate, and pulse pressure but no change in mean arterial blood pressure. The administration of 5 per cent CO2 during the isoproterenol infusion abolished the increase in muscle blood flow, produced an increase in mean arterial blood pressure, and caused an attenuation of the chronotropic effect of isoproterenol. These results suggest that certain cardiovascular effects of isoproterenol are altered during respiratory acidosis.

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Section: Discussionsupporting

confidence: 91%

Section: Departments Of Medicine and Pharmacology Royal Free Hospitamentioning

confidence: 97%

The effect of five per cent carbon dioxide on the response of muscle blood flow to isoproterenol in man

Xanalatos¹,

MacDonell²,

Larbi³

et al. 1973

Clin Pharma and Therapeutics

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“…However, there was not such a large rise in flow with noradrenaline as isoprenaline. When CO2 was administered during the isoprenaline infusion, cerebral blood flow fell to control levels, whereas when given during the Since it has been shown that many ,B-adrenergic effects are abolished or attenuated by administration of CO2 (Schroeder, Robinson, Miller & Harrison, 1970;Xanalatos & James, 1972) and also that some of the effects of noradrenaline (such as those on the heart) are ,3-effects (Benfey & Varma, 1964;Brick, Hutchinson & Roddie, 1966a,b) it was decided that the effect of noradrenaline infusion following the prior administration of the ,B-adrenoceptor blocking agent, propranolol, should be evaluated.…”

Section: Discussionmentioning

confidence: 99%

Factors Affecting the Cerebrovascular Response to Noradrenaline in the Dog

James

MacDonell

1975

British J Pharmacology

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1Noradrenaline infused into the internal carotid artery of the dog (0.01-1 Mg kg-' min-)constricts the blood vessels of the cortex. This constriction is mediated by the action of noradrenaline on a-adrenoceptors of the cerebral arteries.2 Intravenous (1 ,g kg-' min-) or intra common carotid arterial (0.01-1 Mg kg-' min-) infusions of noradrenaline cause an increase in cortical blood flow that can be dissociated from changes in blood pressure. 3 The effect of intravenous noradrenaline on the cortical blood vessels and metabolism is blocked by high Paco2 levels, or by the prior administration of (+)-propranolol. (+)-Propranolol is without such effect. 4 Following section of both vagi and both sinus nerves, intravenous noradrenaline fails to cause an increase in cortical blood flow. 5 In another series of animals the area of the carotid bifurcation was vascularly isolated and perfused with blood from a second dog. Chemoreceptor and baroreceptor activity was shown to be intact. 6 Administration of 5% CO2 to the donor dog caused an increase in cerebral blood flow in the recipient dog. 9 This evidence suggests that the cerebrovasodilatation observed following intravenous noradrenaline is reflex and is triggered by chemoreceptor activity. 10 The evidence also suggests that the antagonism of the cortical dilatory effects of intravenous noradrenaline by raised Paco2 in the intact animal must be at a site different from the peripheral chemoreceptors.

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“…Studies from our laboratories have shown that dogs of this size ventilated at the stated volume and rate developed respiratory hypercapnia and acidosis (unpublished data). Other studies from this laboratory have shown that heart rate varies directly with pC02; therefore, we would suggest that the decreases in heart rate observed in these studies was due to hypercapnia, rather than to the effects of morphine (5).…”

Section: 6%mentioning

confidence: 55%

Circulatory Effects of Morphine Sulfate Following Experimental Myocardial Infarction

Hamilton

Paaso

Corday

et al. 1971

Experimental Biology and Medicine

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Although morphine sulfate is commonly administered to patients with acute myocardial infarction there are few controlled studies dealing with the circulatory effects of morphine after acute myocardial infarction, In aln uncontrolled study in man, Thomas et al. (1) studied 13 patients with acute myocardial infarction of varying severity and found that intravenously adlministered morphine produced varying effects on heart rate, blood pressure, pulse pressure, and cardiac output, depending on the pretreatment circulatory status of the patients. Vasko e.t al.( 2 ) reported on the mechanism of action of morphine in the treatment of experimentally produced acute pulmonary edema, including acute pulmonary edema secondary to myocardial infarction, but did not report the circulatory effects of morphine in acute myocardial infarction without pulmonary edema. In addition, their studies were made in a right heart bypass preparation which did not allow study of the enthe circulatory effects of (morphine.Accordingly our studies were designed to define the effects of morphine on the heart and circulation after acute myocardial infarction.Methods. Twenty-one mongrel dogs ranging in weight from 12 to 30 kg were anesthetized with a mixture of alpha-chloralose and urethane, 66 and 400 mgJkg, respectively. Artificial ventilation was maintained and supplemental anesthetic was administered during the procedure as necessary.A sternum-spli tting midline bhoracotomy These studies were supported in part by NIH Grants Nos. HE 09058, HE 05709, HE 05866; a grant from the American Heart Association, No. 708; and a grant from the National Aeronautics & Space Administration, No. 05 020 305.was performed and the tidal volume of the respirator was adjusted to provide complete expansion of the lungs. Arterial blood pH and p02 were analyzed frequently during each procedure and the tidal volume and respiratory rate were adjusted to maintain blood pH at 7.40 t 0.05 and arterial oxygen tension at 95 t 10 mm Hg. Fluid filled polyethylene catheters (PE-240) were inserted into the right atrium, left atrium, left ventricle, and ascending aorta. Catheters were colnnected to Statham P23Db transducers and pressures recorded on a Beckman Model R directwriting oscillograph. Mean aortic blood flow was measured with a gated sine-wave electromagnetic flowmeter (Biotronics, Silver Spring, Maryland); the flow probe was positioned around the ascending aorta immediately above the takeo'ff of the coronary arteries. The systemic vascular resistance was calculated by the formula: systemic vascular resistance = (mean aortic pressureright atrial pressure) /cardiac output (liters/min) . Myocardial contractility was estimated by measurement of the maximal rate of pressure rise in the left ventricle (LV d p / d t ) recorded directly from the left ventricular pressure by means of an RC differentiating circuit; the frequency response of this system averaged 30 CPS. The left ventricular catheter was made of stiff polyethylene and was 50 cm in length. Electrocardiographic lead ...

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Effects of respiratory acidosis on circulatory response to isoproterenol

Cited by 14 publications

References 0 publications

The effect of five per cent carbon dioxide on the response of muscle blood flow to isoproterenol in man

The effect of five per cent carbon dioxide on the response of muscle blood flow to isoproterenol in man

Factors Affecting the Cerebrovascular Response to Noradrenaline in the Dog

Circulatory Effects of Morphine Sulfate Following Experimental Myocardial Infarction

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