Studies on the Regulation of Respiration in Acute Hypoxia: With an Appendix on Kespiratory (Control During Prolonged Hypoxia

Nielsen, Marius; Smith, H.

doi:10.1111/j.1748-1716.1952.tb00847.x

Cited by 268 publications

(39 citation statements)

References 27 publications

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“…Since hypoxia and hypercapnia interact, this effect will be most STEADY-STATE AND PROGRESSIVE HYPOXIA apparent at high levels of ventilation, such as those provoked by PCO, levels close to control mixed venous Pco,. Furthermore, several authors (Weil & Zwillich, 1976; Kronenberg, Hamilton, Gabel, Hickey, Read & Severinghaus, 1972;Nielsen & Smith, 1952) , and with studies of Gautier using cats (Gautier, 1975) and Cherniack with conscious goats (N. S. Cherniack, unpublished work) but appears to contrast with the findings of Jennett, et al (1974) and…”

Section: Discussioncontrasting

confidence: 44%

Influence of rate of induction of hypoxia on the ventilatory response

Mahutte

Rěbuck

1978

The Journal of Physiology

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Section: Discussioncontrasting

confidence: 44%

Influence of rate of induction of hypoxia on the ventilatory response

Mahutte

Rěbuck

1978

The Journal of Physiology

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“…If indeed chemoreflexes participate in the f H reduction and SBP increase in 3, as previously suggested (Foster and Sheel, 2005;Perini et al, 2008Perini et al, , 2010, a central role must be played by the progressive increase in CO 2 stores. The sensitivity of the ventilatory response to CO 2 is much higher than that of the ventilatory responses to hypoxia (Nielsen and Smith, 1952). This suggests that relatively modest increases in PCO 2 might be sufficient to elicit diaphragmatic contractions.…”

Section: The Effects Of Oxygen Breathing On the Cardiovascular Responmentioning

confidence: 77%

Cardiovascular responses to dry resting apnoeas in elite divers while breathing pure oxygen

Fagoni

Sivieri

Antonutto

et al. 2015

Respiratory Physiology & Neurobiology

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a b s t r a c tPurpose: We hypothesized that the third dynamic phase ( 3) of the cardiovascular response to apnoea requires attainment of the physiological breaking point, so that the duration of the second steady phase ( 2) of the classical cardiovascular response to apnoea, though appearing in both air and oxygen, is longer in oxygen. Methods: Nineteen divers performed maximal apnoeas in air and oxygen. We measured beat-by-beat arterial pressure, heart rate (f H ), stroke volume (SV), cardiac output (Q ). Results: The f H , SV andQ changes during apnoea followed the same patterns in oxygen as in air. Duration of steady 2 was 105 ± 37 and 185 ± 36 s, in air and oxygen (p < 0.05), respectively. At end of apnoea, arterial oxygen saturation was 1.00 ± 0.00 in oxygen and 0.75 ± 0.10 in air. Conclusions:The results support the tested hypothesis. Lack of hypoxaemia during oxygen apnoeas suggests that, if chemoreflexes determine 3, the increase in CO 2 stores might play a central role in eliciting their activation.

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“…These findings on the reflex responses from the aortic bodies fall into line, therefore, with those of Otey & Bernthal (1960) who observed a similar phenomenon measuring respiratory responses to stimulation of the carotid bodies, and agree with the views of Joels & Neil (1961) and Neil & Joels (1963), based on studies of the chemoreceptor impulse discharge from the carotid bodies. These findings may explain, at least in part, the fact that in man the respiratory response to a given rise of arterial Pco2 is increased by hypoxia (Nielsen & Smith, 1951;Lloyd, Jukes & Cunningham, 1958). SUMMARY 1.…”

mentioning

confidence: 92%