Experimental Studies on Rapid Breathing

Binger, Carl A. L.; Brow, G. R.; Branch, Arnold

doi:10.1172/jci100008

Cited by 34 publications

(3 citation statements)

References 7 publications

(13 reference statements)

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“…As a precaution against the loss of heat each animal was wrapped snugly in woolen blankets and surrounded by warm air. 2 When the animal had reached the desired state of anesthesia, tracheotomy was done, and a properly fitting rubber tube was tied firmly into the trachea. This tube, which was of such a length as not to increase the dog's natural dead space, communicated with one arm of a four-way metal tube.…”

Section: Methodmentioning

confidence: 99%

“…A study of these effects in animals was undertaken by us with several points in mind. We hoped for additional information as to the nature and origin of rapid and shallow breathing, which we have previously considered in both clinical and experimental studies (2)(3)(4)(5). It seemed highly desirable to learn something about the liability to fatigue of so vital a structure as the respiratory center.…”

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confidence: 99%

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The Response to Respiratory Resistance

Moore

Binger

1927

Journal of Experimental Medicine

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The liability to fatigue of the respiratory center is a subject which needs to be studied. Davies, Haldane, and Priestley (1) were the first to investigate the manner in which breathing adapts itself to increased resistance, and the point at which the adaptation begins to fail. They showed that the normal response in man to respiratory resistance in both phases of respiration is slow and deep breathing. When the resistance is excessive respirations become progressively shallower and more frequent and the subjects then become cyanotic. Haldane and his coworkers believe that this is due to fatigue of the respiratory center. They believe anoxemia hastens greatly the onset of fatigue and the ease with which it is produced. They conclude that the mechanism involved in the immediate response is the HeringBreuer reflex, pointing out that as a result of resistance, the time required for inflation or deflation of the lungs to reach the point at which the Hering-Breuer stimulus becomes effective is prolonged, that CO~ accumulates in the meantime, and that the next respiration is deep and vigorous. The more or less sudden onset of rapid, shallow breathing Haldane interprets as evidence of fatigue of the respiratory center, with a resulting predominance of the peripheral stimuli over the central impulses normally governing breathing.A study of these effects in animals was undertaken by us with several points in mind. We hoped for additional information as to the nature and origin of rapid and shallow breathing, which we have previously considered in both clinical and experimental studies (2-5). It seemed highly desirable to learn something about the liability to fatigue of so vital a structure as the respiratory center. Transferring the problem

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Section: Methodmentioning

confidence: 99%

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confidence: 99%

The Response to Respiratory Resistance

Moore

Binger

1927

Journal of Experimental Medicine

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“…That abnormalities of ventilation are associated with platelet activation has been known for many years; it is manifested in various pulmonary pathophysiologic settings, which include massive platelet activation, such as in PE. Almost a century ago, Binger et al reported that freezing of the vagus nerves converted the rapid shallow breathing associated with acute PE to slow deep breathing [ 30 ]. Since then, numerous studies in different animal models have implicated the vagus nerve not only in rapid shallow breathing but also in the bronchoconstriction observed during the early phases of PE (see e.g.…”

Section: Platelet Activation Atp and Vagal Stimulationmentioning

confidence: 99%

Adenosine 5’-triphosphate’s role in bradycardia and syncope associated with pulmonary embolism

2018

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Adenosine 5′-triphiosphate (ATP) is released from cells under physiologic and pathophysiologic conditions. Extracellular ATP acts as an autocrine and paracrine agent affecting various cell types by activating cell surface P2 receptors (P2R), which include trans-cell membrane cationic channels, P2XR, and G protein coupled receptors, P2YR. We have previously shown that ATP stimulates vagal afferent nerve terminals in the lungs by activating P2X2/3R. This action could lead to bronchoconstriction, cough and the local release of pro-inflammatory neuropeptides. In addition, ATP markedly enhances the IgE-dependent histamine release from human lung mast cells. Thus, we have proposed for the first time that extracellular ATP plays a mechanistic role in pulmonary pathophysiology in general and chronic obstructive pulmonary disease (COPD), and acute bronchoconstriction in asthma in particular. The present review examines whether ATP could also play a role in bradycardia and syncope in a subset of patients with pulmonary embolism.

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Factors Causing Clinical Jaundice in Heart Disease

Kugel¹,

Lichtman²

1933

Arch Intern Med

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Experimental Studies on Rapid Breathing

Cited by 34 publications

References 7 publications

The Response to Respiratory Resistance

The Response to Respiratory Resistance

Adenosine 5’-triphosphate’s role in bradycardia and syncope associated with pulmonary embolism

Factors Causing Clinical Jaundice in Heart Disease

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