Apneustic breathing after vagotomy in cats with chronic pneumotaxic center lesions

John, Walter M. St.; Glasser, Richard; Richard, A

doi:10.1016/0034-5687(71)90056-9

Cited by 70 publications

(12 citation statements)

References 21 publications

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“…When the pneumotaxic center has a lesion, disinhibition of the apneustic center results in tonic activation of the inspiratory drive and a prolonged inspiratory pause. This traditional model was supported by other authors (Stella 1938, St John et al 1971, von Euler et al 1976, Caille et al 1981, Ling et al 1994, Morrison et al 1994) and the function of the pneumotaxic center, which is believed to be located in the medial parabrachial and Kölliker-Fuse nuclei in pontine tegmentum, has been confirmed (Foutz et al 1988, Feldman et al 1992, Ling et al 1994. In asphyxiated children with brainstem involvement, the tegmentum areas are often more vulnerable (Myers 1975, Leech et al 1988, Roland et al 1988, and this might Case Report 565 explain the presence of apneusis in our subjects.…”

Section: Discussionsupporting

confidence: 58%

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Apneustic breathing in children with brainstem damage due to hypoxic–ischemic encephalopathy

Saito¹,

Hashimoto²,

Iwata³

et al. 1999

Develop Med Child Neuro

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To confirm the presence of apneusis in patients with hypoxic–ischemic encephalopathy and to clarify which factors influence their respiratory patterns, polygraphic studies were performed on two patients. Apneusis was clinically suspected in both patients who had severe brainstem damage. In one subject, inputs of vagal afferents from the gastrointestinal tract and the urinary bladder often resulted in extreme tachypnea instead of apneusis. Lung inflation facilitated expiration during inspiratory arrest. Expiration preceded a periodic inhibition of rigospastic discharge in the right biceps muscle. In the other subject, prolonged inspiratory pauses with cyanosis occurred with or without preceding epileptic seizure. Both phenytoin dose reduction and treatment with tandospirone, a serotonin‐1A agonist, were effective in improving the respiratory distress in this subject.

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Section: Discussionsupporting

confidence: 58%

“…Blockade of vagal inputs is often critical in animal experiments to establish apneusis (St John et al 1971, von Euler et al 1976, Caille et al 1981, Foutz et al 1988). In subject 1, when reducing the rate of mechanical ventilation, lung inflation by the ventilator provoked spontaneous expiration.…”

Section: Discussionmentioning

confidence: 99%

Apneustic breathing in children with brainstem damage due to hypoxic–ischemic encephalopathy

Saito¹,

Hashimoto²,

Iwata³

et al. 1999

Develop Med Child Neuro

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“…8 summarizes some of their findings and demonstrates their approach. RTN neurons that respond to CO 2 /H + in vitro and in vivo express the glutamate transporter VGLUT2 and the autonomic nervous system fate determining gene, Phox2b (118, 242), and some RTN neurons also express galanin (243). This phenotype characterization has led to the development of interesting ideas regarding chemoreception and the RTN and to experiments in vivo that alter the function of these specific neurons.…”

Section: The Location Of Central Chemoreceptorsmentioning

confidence: 99%

Central Chemoreceptors: Locations and Functions

Nattie¹,

Li²

2012

Comprehensive Physiology

203

139

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Central chemoreception traditionally refers to a change in ventilation attributable to changes in CO2/H+ detected within the brain. Interest in central chemoreception has grown substantially since the previous Handbook of Physiology published in 1986. Initially, central chemoreception was localized to areas on the ventral medullary surface, a hypothesis complemented by the recent identification of neurons with specific phenotypes near one of these areas as putative chemoreceptor cells. However, there is substantial evidence that many sites participate in central chemoreception some located at a distance from the ventral medulla. Functionally, central chemoreception, via the sensing of brain interstitial fluid H+, serves to detect and integrate information on 1) alveolar ventilation (arterial PCO2), 2) brain blood flow and metabolism and 3) acid-base balance, and, in response, can affect breathing, airway resistance, blood pressure (sympathetic tone) and arousal. In addition, central chemoreception provides a tonic ‘drive’ (source of excitation) at the normal, baseline PCO2 level that maintains a degree of functional connectivity among brainstem respiratory neurons necessary to produce eupneic breathing. Central chemoreception responds to small variations in PCO2 to regulate normal gas exchange and to large changes in PCO2 to minimize acid-base changes. Central chemoreceptor sites vary in function with sex and with development. From an evolutionary perspective, central chemoreception grew out of the demands posed by air vs. water breathing, homeothermy, sleep, optimization of the work of breathing with the ‘ideal’ arterial PCO2, and the maintenance of the appropriate pH at 37°C for optimal protein structure and function.

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“…Studies using c-Fos-immunoreactive expression as a marker of neuronal activity showed intense activation of the KF region after hypoxia, hypercapnia, or stimulation of the carotid sinus nerve (3, 5, 29, 61). Studies in cats and rats showed that after bilateral lesions of the parabrachial and the Kölliker-Fuse complex, the breathing increase during hypoxia or hypercapnia was attenuated (29,38,(55)(56)(57).However, most of the experiments showing the role of the pontine regions in viscerosensory control consider the parabrachial complex as a unique brain structure involved in different physiological functions, including breathing and autonomic regulation. Therefore, the main goal of this study was to determine the involvement of the KF and the LPBN in the resting respiratory rhythm and cardiorespiratory responses elicited by chemoreceptor activation in unanesthetized rats.…”

mentioning

confidence: 92%

mentioning

confidence: 98%

Regulation of the chemosensory control of breathing by Kölliker-Fuse neurons

Damasceno

Takakura

Moreira

2014

American Journal of Physiology-Regulatory, Integrative and Comp

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The Kölliker-Fuse region (KF) and the lateral parabrachial nucleus (LPBN) have been implicated in the maintenance of cardiorespiratory control. Here, we evaluated the involvement of the KF region and the LPBN in cardiorespiratory responses elicited by chemoreceptor activation in unanesthetized rats. Male Wistar rats (280-330 g; n = 5-9/group) with bilateral stainless-steel guide cannulas implanted in the KF region or the LPBN were used. Injection of muscimol (100 and 200 pmol/100 nl) in the KF region decreased resting ventilation (1,140 ± 68 and 978 ± 100 vs. saline: 1,436 ± 155 ml·kg(-1)·min(-1)), without changing mean arterial pressure (MAP) and heart rate (HR). Bilateral injection of the GABA-A antagonist bicuculline (1 nmol/100 nl) in the KF blocked the inhibitory effect on ventilation (1,418 ± 138 vs. muscimol: 978 ± 100 ml·kg(-1)·min(-1)) elicited by muscimol. Muscimol injection in the KF reduced the increase in ventilation produced by hypoxia (8% O2) (1,827 ± 61 vs. saline: 3,179 ± 325 ml·kg(-1)·min(-1)) or hypercapnia (7% CO2) (1,488 ± 277 vs. saline: 3,539 ± 374 ml·kg(-1)·min(-1)) in unanesthetized rats. Bilateral injection of bicuculline in the KF blocked the decrease in ventilation produced by muscimol in the KF during peripheral or central chemoreflex activation. Bilateral injection of muscimol in the LPBN did not change resting ventilation or the increase in ventilation elicited by hypoxia or hypercapnia. The results of the present study suggest that the KF region, but not the LPBN, has mechanisms to control ventilation in resting, hypoxic, or hypercapnic conditions in unanesthetized rats.

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Apneustic breathing after vagotomy in cats with chronic pneumotaxic center lesions

Cited by 70 publications

References 21 publications

Apneustic breathing in children with brainstem damage due to hypoxic–ischemic encephalopathy

Apneustic breathing in children with brainstem damage due to hypoxic–ischemic encephalopathy

Central Chemoreceptors: Locations and Functions

Regulation of the chemosensory control of breathing by Kölliker-Fuse neurons

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