Anatomical arrangement of hypercapnia-activated cells  in the superficial ventral medulla of rats

Okada, Yasumasa; Chen, Zibin; Jiang, Wuhan; Kuwana, Shun-ichi; Eldridge, Frederíc L.

doi:10.1152/japplphysiol.00620.2000

Cited by 99 publications

(100 citation statements)

References 34 publications

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“…The recent work of Okada et al (35), Ballantyne and Scheid (6), and Richerson et al (37), for example, supports the idea of a perivascular location for many chemosensitive medullary neurons. Older studies have shown, on the basis of medullary surface pH measurements, that pH can change very rapidly, approximating the delay from ventilatory overshoot to apnea (1,16,25).…”

Section: Discussionmentioning

confidence: 86%

Carotid body denervation eliminates apnea in response to transient hypocapnia

Nakayama¹,

Smith²,

Rodman³

et al. 2003

Journal of Applied Physiology

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Section: Discussionmentioning

confidence: 86%

Carotid body denervation eliminates apnea in response to transient hypocapnia

Nakayama¹,

Smith²,

Rodman³

et al. 2003

Journal of Applied Physiology

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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).…”

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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“…The retrotrapezoid nucleus (RTN) contains acid-sensitive glutamatergic interneurons with properties consistent with a central respiratory chemoreceptor function (Akilesh et al 1997;Feldman et al 2003;Guyenet et al 2005b;Mulkey et al 2004;Nattie and Li 2006;Okada et al 2002;Ritucci et al 2005;Rosin et al 2006;. RTN neurons are also activated by carotid body stimulation and inhibited by lung inflation, and these effects are probably mediated via direct projections from solitary tract nucleus (NTS) neurons (Moreira et al 2007;.…”

Section: Introductionmentioning

confidence: 99%

Activation of 5-Hydroxytryptamine Type 3 Receptor-Expressing C-Fiber Vagal Afferents Inhibits Retrotrapezoid Nucleus Chemoreceptors in Rats

Moreira

Takakura²,

Colombari³

et al. 2007

Journal of Neurophysiology

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Moreira TS, Takakura AC, Colombari E, Guyenet PG. Activation of 5-hydroxytryptamine type 3 receptor-expressing C-fiber vagal afferents inhibits retrotrapezoid nucleus chemoreceptors in rats. J Neurophysiol 98: 3627-3637, 2007. First published October 10, 2007 doi:10.1152/jn.00675.2007. Retrotrapezoid nucleus (RTN) chemoreceptors are regulated by inputs from the carotid bodies (CB) and from pulmonary mechanoreceptors. Here we tested whether RTN neurons are influenced by 5-hydroxytryptamine type 3 receptor-expressing C-fiber vagal afferents. In urethan-anesthetized rats, selective activation of vagal C-fiber afferents by phenylbiguanide (PBG) eliminated the phrenic nerve discharge (PND) and inhibited RTN neurons (n ϭ 24). PBG had no inhibitory effect in vagotomized rats. Muscimol injection into the solitary tract nucleus, commissural part, reduced inhibition of PND and RTN by PBG (73%), blocked activation of PND and RTN by CB stimulation (cyanide) but had no effect on inhibition of PND and RTN by lung inflation. Bilateral injections of muscimol into interstitial solitary tract nucleus (NTS) reduced the inhibition of PND and RTN by PBG (53%), blocked the inhibitory effects of lung inflation but did not change the activation of PND and RTN neurons by CB stimulation. PBG and lung inflation activated postinspiratory neurons located within the rostral ventral respiratory group (rVRG) and inhibited inspiratory and expiratory neurons. Bilateral injections of muscimol into rVRG eliminated PND and partially decreased RTN neuron inhibition by PBG (32%). In conclusion, activation of cardiopulmonary C-fiber afferents inhibits the activity of RTN chemoreceptors. The pathway relays within a broad medial region of the NTS and involves the rVRG to a limited degree. The apnea triggered by activation of cardiopulmonary C-fiber afferents may be due in part to a reduction of the activity of RTN chemoreceptors.

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Anatomical arrangement of hypercapnia-activated cells in the superficial ventral medulla of rats

Cited by 99 publications

References 34 publications

Carotid body denervation eliminates apnea in response to transient hypocapnia

Carotid body denervation eliminates apnea in response to transient hypocapnia

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

Activation of 5-Hydroxytryptamine Type 3 Receptor-Expressing C-Fiber Vagal Afferents Inhibits Retrotrapezoid Nucleus Chemoreceptors in Rats

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