Evidence for the Role of Humoral Mechanisms in the Cardiovascular Responses to Hypoxia and Anaemia

Hatcher, John M.; Jennings, D. B.

doi:10.1159/000389576

Cited by 6 publications

(6 citation statements)

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“…Hypoxia is a stress which causes the release of catecholamines, the development of acidosis and eventual death (Von Euler and Lishajko, 1963;Hatcher and Jennings, 1966;Nahas et al, 1967). Propranolol improved the survival of animals that had severe acidosis and increased catecholamine concentrations in association with posthaemorrhagic shock (Berk et al, 1967;Halmagyi, Irving and Varga, 1968).…”

Section: Discussionmentioning

confidence: 99%

“…The oxygen stores of the body are limited, and the margin of safety during hypoxia is small. Hypoxia causes acidosis and the release of catecholamines from peripheral nerve endings and the adrenal glands (Von Euler and Lishajko, 1963;Hatcher and Jennings, 1966;Nahas et al, 1967). Increases in the concentrations of circulating catecholamines increase further the demand for oxygen and perpetuate the downhill spiral.…”

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confidence: 99%

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Propranolol Increases Oxygen Utilization During Hypoxia

Khambatta¹,

Stone²,

Askanazi³

et al. 1987

British Journal of Anaesthesia

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The effects of propranolol on whole body oxygen consumption and blood oxygen content were measured in the dog during extreme hypoxic conditions. At 9% inspired oxygen four of eight control animals died within 40 min. An identical second group was pretreated with propranolol and none died during the same hypoxic stress. Hypoxia decreased oxygen consumption in both groups, but the decrease was less in the propranolol-pretreated dogs. A second set of 16 dogs was ventilated with 10% oxygen and all animals survived. A similar, although less pronounced, effect on oxygen consumption was noted and propranolol once again lessened the hypoxia-induced decrease in oxygen consumption. With hypoxaemia, metabolic acidosis developed in all animals and the arterio-venous oxygen content difference decreased; however, propranolol lessened the acidosis and the decrease in arterio-venous oxygen content difference. We conclude that, during hypoxia, propranolol increases oxygen utilization by the tissues and this might account for better survival.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Propranolol Increases Oxygen Utilization During Hypoxia

Khambatta¹,

Stone²,

Askanazi³

et al. 1987

British Journal of Anaesthesia

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“…Acute hypoxia in normal man and in animals causes tachycardia. The accu mulated evidence suggests that this is due to a direct action in the brain, resulting in increased sympathetic activity; this may stimulate the pacemaker both through its sympathetic nerve supply (Downing, 1966) and by means of increased adrenal medullary secretion (Hatcher & Jennings, 1966). There is also increased cardiac output, but not, in man, an increase in arterial blood pressure: vasomotor activity is countered by peripheral vasodilatation particularly in skeletal muscle, as a direct effect of hypoxaemia (Black & Roddie, 1958;Richardson, Kontos, Raper & Patterson, 1967).…”

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confidence: 99%

The response of heart rate to hypoxia in man after cervical spinal cord transection

Jennett

1970

Spinal Cord

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“…The consensus of opinion is that the maintenance of enhanced cardiac performance during longer periods of moderately severe hypoxia is a function of catecholamines secreted by the adrenal medulla (Kontos and Lower, 1969;Chiong and Hatcher, 1972). The previous administration of beta-adrenergic drugs has been shown to reduce greatly the cardiovascular response to hypoxia (Hatcher and Jennings, 1966;Daugherty, Scott and Haddy, 1967;Krasney, 1967;Kontos and Lower, 1969). Malik and Langford-Kidd (1973), however, were unable to demonstrate any effect of propranolol 2.0 mg/kg i.v.…”

Section: Discussionmentioning

confidence: 99%

Haemodynamic Interactions of High-Dose Propranolol Pretreatment and Anaesthesia in the Dog Ii: The Effects of Acute Arterial Hypoxaemia at Increasing Depths of Halothane Anaesthesia

Roberts

Foëx

Clarke

et al. 1976

British Journal of Anaesthesia

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Beta-adrenergic blockade may impair the normal cardiovascular response to hypoxia occurring during general anaesthesia. The haemodynamic effects of acute hypoxia, induced by a 90-s period of ventilation with nitrogen, were studied during increasing depths of halothane anaesthesia up to a maximum of 2.5% inspired halothane in dogs chronically implanted with intracardiac catheters, a left-ventricular pressure transducer and an aortic blood flow transducer. An untreated group of dogs and a group which had been treated for 3 weeks with propranolol 20 mg/kg/day were compared. The beta-blocked group had lesser cardiac output values, left-ventricular contractility indices, external left-ventricular work and peak left-ventricular power at all depths of anaesthesia except 2.5% halothane, but both groups responded to hypoxia similarly at each depth of anaesthesia. Cardiac performance was enhanced in both groups during acute hypoxia. No adverse haemodynamic effect of the combination of propranolol, halothane and hypoxia was demonstrated.

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Evidence for the Role of Humoral Mechanisms in the Cardiovascular Responses to Hypoxia and Anaemia

Cited by 6 publications

References 0 publications

Propranolol Increases Oxygen Utilization During Hypoxia

Propranolol Increases Oxygen Utilization During Hypoxia

The response of heart rate to hypoxia in man after cervical spinal cord transection

Haemodynamic Interactions of High-Dose Propranolol Pretreatment and Anaesthesia in the Dog Ii: The Effects of Acute Arterial Hypoxaemia at Increasing Depths of Halothane Anaesthesia

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