The Influence of Short Periods of Induced Acute Anoxia Upon Pulmonary Artery Pressures in Man

Motley, Hurley L.; Cournand, André; Werkö, Lars; Himmelstein, Aaron; Dresdale, David T.

doi:10.1152/ajplegacy.1947.150.2.315

Cited by 404 publications

(121 citation statements)

References 0 publications

Supporting

Mentioning

112

Contrasting

Unclassified

Order By: Relevance

“…278,279 However, there is debate as to whether OSA can be a primary cause of sustained pulmonary arterial hypertension. The most direct evidence comes from observations that treatment of OSA with CPAP may lower daytime pulmonary artery pressure.…”

Section: Osa and The Origin And Progression Of Pulmonary Arterial Hypmentioning

confidence: 99%

Sleep Apnea and Cardiovascular Disease

et al. 2008

View full text Add to dashboard Cite

Section: Osa and The Origin And Progression Of Pulmonary Arterial Hypmentioning

confidence: 99%

Sleep Apnea and Cardiovascular Disease

et al. 2008

View full text Add to dashboard Cite

“…L.O., and A.G.) were subjected to acute hypoxia after 2 con-secutive periods of exercise anid a second control period. The data for the normal subjects are contained in tables 1, 2, 4, and 5; the pertinent data for the 3 patients are listed in table 6. At equivalent levels of cardiac output, the normal subjects manifested higher pulmonary artery pressures during hypoxia than during exercise (fig.…”

Section: Resultsmentioning

confidence: 99%

Effects of Acute Hypoxia and Exercise on the Pulmonary Circulation

1960

View full text Add to dashboard Cite

MAJOR obstacles complicate the study of the pulmonary circulation in man: the inaccessibility of the pulmonary vessels for direct cannulation, and the multiplicity of extravascular factors that influence pressure-flow-volume relationships within the lungs. New technics have largely circumvented the first difficulty; the second difficulty is minimal in the normal resting subject, but is exaggerated by either physiologic stress, e.g., exercise, or by abnormalities of the heart or lungs.Observations on a variety of experimental preparations have afforded considerable insight into the regulation of the pulmonary circulation. Particularly rewarding have been the demonstrations by Beyne in the dog' and by von Euler and Liljestrand in the cat,2-4 that acute hypoxia, hypereapnia, or both elicit pulmonary hypertension. These observations constitute a landmark in studies of the regulation of the pulmonary circulation since they afforded an experimental tool for the production of a pulmonary pressor response, and provided a hypothesis,2-4 which could be tested, concerning the adaptation of pulmonary capillary perfusion to alveolar ventilation. Others have subsequently reproduced the pressor response to acute hypoxia in animals5 and in man ;6 attempts to reproduce the pulmonary pressor response to acute hypercapnia have yielded far less consistent results.7The present studies were designed to eluci- report compares the effects of acute hypoxia and of exercise on pressure-flow relationships in normal subjects, in patients with restricted vascular beds, and in a patient with sympathetic denervation of the lungs. The second paper, because of the special technics involved, is confined to the effects of acute hypoxia on the pulmonary blood volume. The third considers the effects of acute hypereapnia on pressure-flow relationships in the pulmonary circulation.Methods All patients underwent a preliminary period of adjustment to the laboratory, its personnel, and facsimiles of the experimental protocol; this consisted of trial runs on a variety of hypoxic breathing mixtures coupled with collections of arterial blood and expired gas. Those who tolerated these procedures well subsequently served as experimental subjects.All tests were performed in the postabsorptive state, without medication. Venous catheterization of the right heart was performed in the usual manner8 and the tip of the catheter was placed in the pulmonary artery. The combination of the right heart catheterization, arterial cannulation, and the open-circuit method for collection of expired gas supplied the samples necessary for the calculation of the oxygen uptake (Vo,), the respiratory exchange ratio (RE), and the cardiac output (Q) by application of the Fick principle.For the recording of pulmonary and systemic arterial pressures, Statham gages were used as pressure transducers, in conjunction with highsensitivity carrier amplifiers and photographic registration of the cathode-ray images.The protocols were designed to satisfy criteria for the "steady state."9 In br...

show abstract

“…Motley et al (13), in the laboratory of André Cournand ( Fig. 1) at Bellevue Hospital, aware of the recent observations by Euler and Liljestrand on anesthetized cats, undertook similar observations on five normal human subjects.…”

mentioning

confidence: 76%

Acute hypoxia and pulmonary vasoconstriction in humans: uncovering the mechanism of the pressor response

Fishman

2004

American Journal of Physiology-Lung Cellular and Molecular Phys

View full text Add to dashboard Cite

This essay looks at the historical significance of an APS classic paper that is freely available online:Motley HL, Cournand A, Werko L, Himmelstein A, and Dresdale D. The influence of short periods of induced acute anoxia upon pulmonary artery pressures in man. Am J Physiol 150: 315-320, 1947 (http://ajplegacy.physiology.org/cgi/ reprint/150/2/315).FOR THE LUNGS TO OPERATE EFFICIENTLY in gas exchange, it is essential for the pulmonary blood flow to be directed to well-ventilated areas of the lungs. Teleologically, one mechanism to accomplish this end might be via nerves and pulmonary reflexogenic zones comparable to the sinus and aortic bodies in the systemic circulation. Although the lungs are richly innervated, no evidence indicates that such zones exist or that the nerves to the lungs play such a role. Instead, a mechanism for the control of the distribution of blood within the lungs is hypoxic pulmonary vasoconstriction, which automatically increases pulmonary vascular resistance in poorly aerated regions of the lungs, thereby redirecting pulmonary blood flow to regions richer in oxygen content.A first step in uncovering the existence of hypoxic pulmonary vasoconstriction was taken by Euler and Liljestrand (6, 10). In closed-chest, spontaneously breathing cats anesthetized with chloralose, they showed that acute hypoxia elicits pulmonary vasoconstriction (Fig. 2). They postulated that hypoxic pulmonary vasoconstriction is a mechanism that sustains oxygen delivery to systemic tissues and organs by diverting pulmonary blood flow to the better aerated parts of the lungs. This demonstration, which they supplemented by observations on the effects of muscular work and vasoactive drugs on pulmonary arterial pressures, led to the conclusion that the distribution of the pulmonary blood flow within the lungs is regulated primarily by a local vasomotor mechanism that automatically directs the blood to better ventilated parts of the lungs.Motley et al. (13), in the laboratory of André Cournand (Fig. 1) at Bellevue Hospital, aware of the recent observations by Euler and Liljestrand on anesthetized cats, undertook similar observations on five normal human subjects. The subjects were rendered hypoxic by breathing an inspired gas mixture of 10% O 2 in N 2 for 10 min. In each subject, acute hypoxia elicited pulmonary vasoconstriction, as indicated by an increase in pulmonary arterial pressure. The demonstration of the hypoxic pulmonary pressor response in unanesthetized humans breathing spontaneously represented a landmark in the growth of understanding of the regulation of pulmonary circulation.Unexpectedly, they found that the pulmonary arterial pressor effect was accompanied by a decrease in cardiac output, which they calculated by the Fick principle. However, this decrease in calculated cardiac output during acute hypoxia proved later to be in error (8), due to failure to allow sufficient time for the subjects to reach the steady state of the respiration and circulation required for a valid application of the Fick prin...

show abstract

The Influence of Short Periods of Induced Acute Anoxia Upon Pulmonary Artery Pressures in Man

Cited by 404 publications

References 0 publications

Sleep Apnea and Cardiovascular Disease

Sleep Apnea and Cardiovascular Disease

Effects of Acute Hypoxia and Exercise on the Pulmonary Circulation

Acute hypoxia and pulmonary vasoconstriction in humans: uncovering the mechanism of the pressor response

Contact Info

Product

Resources

About