Studies on the Regulation of Respiration in Acute Hypoxia

Nielsen, Marius; Smith, H.

doi:10.1111/j.1748-1716.1951.tb00748.x

Cited by 120 publications

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“…Hypoxia is known to increase the responsiveness of the peripheral chemoreceptor to CO 2 (20,42), and to reduce the PCO 2 and the H ϩ concentration ([H ϩ ]) at the central chemoreceptors (CC) through its effect of increasing cerebral blood flow (40). In contrast, hyperoxia suppresses peripheral chemoresponsiveness to CO 2 (23) and increases PCO 2 and [H ϩ ] at the sites of central chemoreceptors through reduction of cerebral blood flow (17,21).…”

mentioning

confidence: 99%

Influence of arterial O₂ on the susceptibility to posthyperventilation apnea during sleep

Xie¹,

Skatrud²,

Puleo³

et al. 2006

Journal of Applied Physiology

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Xie, Ailiang, James B. Skatrud, Dominic S. Puleo, and Jerome A. Dempsey. Influence of arterial O2 on the susceptibility to posthyperventilation apnea during sleep. J Appl Physiol 100: 171-177, 2006. First published September 22, 2005 doi:10.1152/japplphysiol.00440.2005.-To investigate the contribution of the peripheral chemoreceptors to the susceptibility to posthyperventilation apnea, we evaluated the time course and magnitude of hypocapnia required to produce apnea at different levels of peripheral chemoreceptor activation produced by exposure to three levels of inspired PO 2. We measured the apneic threshold and the apnea latency in nine normal sleeping subjects in response to augmented breaths during normoxia (room air), hypoxia (arterial O 2 saturation ϭ 78 -80%), and hyperoxia (inspired O2 fraction ϭ 50 -52%). Pressure support mechanical ventilation in the assist mode was employed to introduce a single or multiple numbers of consecutive, sighlike breaths to cause apnea. The apnea latency was measured from the end inspiration of the first augmented breath to the onset of apnea. It was 12.2 Ϯ 1.1 s during normoxia, which was similar to the lung-to-ear circulation delay of 11.7 s in these subjects. Hypoxia shortened the apnea latency (6.3 Ϯ 0.8 s; P Ͻ 0.05), whereas hyperoxia prolonged it (71.5 Ϯ 13.8 s; P Ͻ 0.01). The apneic threshold end-tidal PCO 2 (PETCO 2 ) was defined as the PETCO 2 at the onset of apnea. During hypoxia, the apneic threshold PET CO 2 was higher (38.9 Ϯ 1.7 Torr; P Ͻ 0.01) compared with normoxia (35.8 Ϯ 1.1; Torr); during hyperoxia, it was lower (33.0 Ϯ 0.8 Torr; P Ͻ 0.05). Furthermore, the difference between the eupneic PET CO 2 and apneic threshold PET CO 2 was smaller during hypoxia (3.0 Ϯ 1.0 Torr P Ͻ 001) and greater during hyperoxia (10.6 Ϯ 0.8 Torr; P Ͻ 0.05) compared with normoxia (8.0 Ϯ 0.6 Torr). Correspondingly, the hypocapnic ventilatory response to CO 2 below the eupneic PETCO 2 was increased by hypoxia (3.44 Ϯ 0.63 l ⅐ min Ϫ1 ⅐ Torr Ϫ1 ; P Ͻ 0.05) and decreased by hyperoxia (0.63 Ϯ 0.04 l ⅐ min Ϫ1 ⅐ Torr Ϫ1 ; P Ͻ 0.05) compared with normoxia (0.79 Ϯ 0.05 l ⅐ min Ϫ1 ⅐ Torr Ϫ1 ). These findings indicate that posthyperventilation apnea is initiated by the peripheral chemoreceptors and that the varying susceptibility to apnea during hypoxia vs. hyperoxia is influenced by the relative activity of these receptors. apnea threshold THE RELATIVE CONTRIBUTION of peripheral vs. central chemoreception in initiating the posthyperventilation apneas remains an unresolved question. The importance of peripheral chemoreception in mediating the rapid ventilatory response to hypocapnia has been supported using animal models. Carotid body denervation either eliminated or prolonged the time course for the development of apnea after the administration of augmented breaths (6, 39). However, carotid body denervation profoundly alters central chemoreception as indicated by the substantial CO 2 retention after denervation. Our laboratory has previously demonstrated the complex effect of hypoxia in t...

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confidence: 99%

Influence of arterial O₂ on the susceptibility to posthyperventilation apnea during sleep

Xie¹,

Skatrud²,

Puleo³

et al. 2006

Journal of Applied Physiology

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“…In mammals, interactive effects of O 2 and CO 2 are detectible at the level of ventilation (Nielsen and Smith, 1952), at the level of carotid sinus nerve discharge (Tenney and Brooks, 1966;Daristotle et al, 1987;Lahiri and Delaney, 1975a) and to a very small extent at the level of the increase in intracellular [Ca 2+ ], within the glomus cells, associated with chemoreceptor activation (Bamford et al, 1999;Roy et al, 2000). High levels of CO 2 increase the sensitivity of the carotid body chemoreceptors to low O 2 ; conversely, low levels of O 2 increase the sensitivity of the ventilatory response to hypercapnia (Bamford et al, 1999).…”

Section: Potential Mechanisms Underlying Interactive Effects Between mentioning

confidence: 99%

Reciprocal modulation of O2 and CO2 cardiorespiratory chemoreflexes in the tambaqui

Reid

Perry

Gilmour

et al. 2005

Respiratory Physiology & Neurobiology

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This study examined the effect of acute hypoxic and hypercapnic cardiorespiratory stimuli, superimposed on existing cardiorespiratory disturbances in tambaqui. In their natural habitat, these fish often encounter periods of hypoxic hypercapnia that can be acutely exacerbated by water turnover. Tambaqui were exposed to periods of normoxia, hypoxia, hyperoxia and hypercapnia during which, externally oriented O 2 and CO 2 chemoreceptors were further stimulated, by administration into the inspired water of sodium cyanide and CO 2 -equilibrated water, respectively. Hyperoxic water increased the sensitivity of the NaCN-evoked increase in breathing frequency (f R ) and decrease in heart rate. Hypoxia and hypercapnia attenuated the increase in f R but, aside from blood pressure, did not influence the magnitude of NaCN-evoked cardiovascular changes. Water PO 2 influenced the magnitude of the CO 2 -evoked cardiorespiratory changes and the sensitivity of CO 2 -evoked changes in heart rate and blood flow. The results indicate that existing respiratory disturbances modulate cardiorespiratory responses to further respiratory challenges reflecting both changes in chemosensitivity and the capacity for further change.

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“…Second and most likely, one might regard the ventilation of the animal as an indication ofthe drive level (motivation) existing in neural circuits involved in respiratory control and, if one assumes that this drive level govern:; both the somatic respiratory movements and the learned somatic motor act, then, any factors which tend to activate respiration (via these neural circuits) would also tend to activate the learned motor response. Although the stimulation of the peripheral chemoreceptors by mild hypoxia produces only a small immediate increase in ventilation it !ioes produce a considerable increase in the ventilatory response to C02 (Nielsen, 1952) and thus might be expected to decrease the latent 'period for learned escape (just as would an increast: in CO 2 concentration) .…”

Section: Stephen Arnold Weinstein2mentioning

confidence: 99%

The effect of hypoxia upon learned escape from carbon dioxide

Weinstein

1966

Psychon Sci

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A group of five mice was trained to press a lever to remove 4% C02 from its inspired air. The effect of six levels of hypoxia upon the latent period for learned escape frem the added C02 was determined. Mild hypoxia produced a shortened latent period, severe hypoxia a lengthened latent period. The correlation between the behavioral and ventilatory responses to C02 and hypoxia are discussed.We have previously reported that pigeons are capable of learning to press a switch in order to remove added CO 2 from their inspired air (Weinstein, 196:1, 1964). The amount of time which was taken to press the switch after the onset of the C02 was referred to as the latent period and was shown to be inversely related to the C02 concentration and directly related to the intertrial interval. In the present investigation we have determined the effect of graded levels of hypoxia upon the latent period for learned escape from4% CO 2 , Von Muralt (1964) has discussed the increased sensitivity of sensory mechanisms in mild hypoxia and other investigators have described the enhancement of the ventilatory response to CO 2 in hypoxic environments. Decrements in sensory and motor functions in severe hypoxia are well known and have been extensively described. Gantt (1949) has demonstrated an impairment in conditional reflex formation after exposure to severe hypoxia. On the basis of these findings in other areas, we felt that a systematic investigation to determine the effect of graded hypoxia upon a response which was determined by both stimulus strength and learned central nervous system connections (Weinstein, 1964) would be of interest.The experimental Ss were five white mice of the BALB/c strain. Each mouse had been trained to a pre-determined level of performance in the C02 escape conditioning situation. The criterion for the onset of experimentation was the previous performance of 100 consecutive escape responses from 4% CO 2 in air with no latency greater than 300 sec.The apparatus was a modification of the gas mixing device which we had previously described (Weinstein, 1963).A uniform experimental procedure was utilized for the five animals studied. At the beginning of each experimental day the mouse was placed in the chamber and allowed to rest for 15 min. after which a programming system was turned on. This system activated relays which increased the animal's inspired C02 to 4% with a half time for change of approximately 3 sec. (measured at the end of the chamber most distant from Psychon. Sci., 1966, Vol. 6 (3) STEPHEN ARNOLD WEINSTEIN2JOHNS HOPKINS UNIVERSITY the source of inflow). A timing circuit was activated simultaneously with the increase in CO 2 and the duration of the latent period (time until the escape response) was measured and printed out automatically. The escape response activated another timing circuit which determined the time until the next C02 increase, in this instance 1-1/2 min. Twenty-five trials were carried out in this fashion in a normoxic atmosphere. At the end of this group of trials the atmosph...

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Studies on the Regulation of Respiration in Acute Hypoxia

Cited by 120 publications

References 0 publications

Influence of arterial O₂ on the susceptibility to posthyperventilation apnea during sleep

Influence of arterial O₂ on the susceptibility to posthyperventilation apnea during sleep

Reciprocal modulation of O2 and CO2 cardiorespiratory chemoreflexes in the tambaqui

The effect of hypoxia upon learned escape from carbon dioxide

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