Dynamic respiratory response to abrupt change of inspired CO2 at normal and high PO2.

Gelfand, R; Lambertsen, CJ

doi:10.1152/jappl.1973.35.6.903

Cited by 113 publications

(57 citation statements)

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“…Animal studies indicate that medullary chemoreceptors have a perivascular location (43) and that a decrease in pH of the surface extracellular fluid could be measured only 6 s after CO 2 inhalation in anesthetized cats (40). However, human studies suggested a much longer time delay for the central chemoreceptor response to a change in inspired gases, varying from 20 s (18,24) to ϳ3 min (2,13). In fact, our laboratory's latest study on unanesthetized dog with intact, isolated carotid chemoreceptors shows that the initiation of the ventilatory response to a step increase in PET CO 2 was delayed 1.5-2 times when the carotid chemoreceptor was not exposed to the hypercapnia (47).…”

Section: Discussionmentioning

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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Section: Discussionmentioning

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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“…23,24 Central chemoreceptors, located on the ventral surface of the medulla, respond primarily to hypercapnia. 25 Both these chemoreceptor mechanisms also exert powerful influences on neural circulatory control, especially in situations involving marked changes in arterial oxygen and/or CO 2 . Chemoreflex activation causes increases in sympathetic activity, heart rate (HR), blood pressure, and minute ventilation.…”

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confidence: 99%

Enhanced Sympathetic and Ventilatory Responses to Central Chemoreflex Activation in Heart Failure

et al. 1999

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Background-Sympathetic activation and respiratory abnormalities may each be implicated in the pathophysiology of congestive heart failure (CHF). Chemoreflexes are an important mechanism regulating both sympathetic drive and breathing. We therefore tested the hypothesis that chemoreflex function is altered in CHF. Methods and Results-We compared ventilatory, sympathetic, heart rate, and blood pressure responses to hypoxia, hypercapnia, and the cold pressor test in 9 patients with CHF and 9 control subjects matched for age and body mass index. Baseline muscle sympathetic nerve activity (MSNA) was higher in the patients with CHF compared with control subjects (47Ϯ8 versus 23Ϯ3 bursts per minute, PϽ0.01). During hypercapnia, patients with CHF had greater increases in minute ventilation (6.7Ϯ1.4 versus 2.7Ϯ0.9 L/min, Pϭ0.03) and heart rate (7.0Ϯ2.1 versus 0.6Ϯ1.2 bpm, Pϭ0.02). Despite higher ventilation, which inhibits sympathetic activity, the MSNA increase in patients with CHF was also greater than that in control subjects (58Ϯ12% versus 21Ϯ9%, Pϭ0.03). Ventilatory, autonomic, and blood pressure responses to hypoxia and the cold pressor test in CHF patients were not different from those in control subjects. Conclusions-Chronic heart failure is characterized by a selective potentiation of ventilatory and sympathetic responses to central chemoreceptor activation by hypercapnia. (Circulation. 1999;100:262-267.)

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“…AHMAD and LoESCHCKE (1982) suggested that there must be a difference in the mechanism and/or the location of the process in which C02 stimulation influences f in comparison with those of VT. Namely the difference of the distance between the capillaries and the chemosensory sites or the perfusion rate of the sites may be responsible. A rapid onset off-response suggests that there is a contribution from the peripheral arterial chemoreceptors (BLACK et al, 1971;GELFAND and LAMBERTSEN, 1973). In the present experiments, the carotid sinus nerve was kept intact.…”

Section: Discussionmentioning

confidence: 88%

Delayed ventilatory response to CO2 after carbonic anhydrase inhibition with acetazolamide administration in the anesthetized rat.

1988

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In order to estimate to what extent the stimulatory action of C02 on ventilation is mediated by the formation of H+, we studied effects on the temporal profile of ventilatory response to C02 of carbonic anhydrase (CA) inhibition with acetazolamide in the halothane anesthetized spontaneously breathing rat. Since hydration reaction of C02 yielding H + is delayed by CA inhibition, the time courses of changes in tidal volume (VT), respiratory frequency (f), and minute ventilation (VE) in response to a stepwise increase in end-tidal P~o2 (d PETCo2 15 mmHg) were compared before (control state) and after i.v. injection of acetazolamide (50 mg/kg) in the hyperoxic condition. In the control state, an increase in VT was significantly slower than that in f; and the mean response half-times (T, i2) for the increase in VT, f, and VE were 50.6, 18.1, and 31.0 s, respectively. After acetazolamide administration, responses to C02, especially f -response and consequently 1'E-response became much slower, and the T12 for VT, f, and VE were 67.9, 55.0, and 63.0 s, respectively. The delay in VT-response was not statistically significant. The magnitude of increase in VE in the steady state hypercapnic stimulation was almost the same before and after acetazolamide administration. The results suggest that a rapid increase in f during C02 inhalation occurs predominantly through an increase in H + produced by hydration of C02 with CA, whereas VT-response may occur without involvement of this process. The different time courses of VT-and f -responses and possible effects of molecular C02 and /or H + on the regulatory mechanism for ventilatory pattern were discussed.

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Dynamic respiratory response to abrupt change of inspired CO2 at normal and high PO2.

Cited by 113 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

Enhanced Sympathetic and Ventilatory Responses to Central Chemoreflex Activation in Heart Failure

Delayed ventilatory response to CO2 after carbonic anhydrase inhibition with acetazolamide administration in the anesthetized rat.

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