Pneumotaxic Center | ScienceGate

Ventilatory regulation by pontile pneumotaxic and apneustic centers and by rostral medullary sites was evaluated in intercollicular decerebrate cats. Following pneumotaxic center ablation, PAco2 was significantly elevated.Moreover, in response to hypercapina or hypoxia, frequency responses were significantly diminished whereas tidal volume responses were unchanged or elevated. Interruption of apneustic center function by caudal pontile transection or radiofrequency lesions in the caudal pons and/or rostral medulla resulted in significant decreases of tidal volume responses and significant elevations of frequency responses to both hypercapnia and hypoxia. Neither minute volume responses nor the PAco2 level was altered. It is concluded that the apneustic center exercises a primary role in the brainstem definitionof tidal volume responses for both peripheral and central chemoreceptor afferent stimuli. The apneustic center is also considered to exert an impoetant function in the definition of respiratory frequency. A medially placed pathway in the rostral medulla is proposed to interconnect the apneustic center with the medullary respiratory nuclei.

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Genesis of rhythmic respiratory activity in pons independent of medulla

Journal of Applied Physiology ◽

10.1152/jappl.1985.59.3.684 ◽

1985 ◽

Vol 59 (3) ◽

pp. 684-690 ◽

Cited By ~ 22

Author(s):

W. M. St John ◽

T. A. Bledsoe

Keyword(s):

Brain Stem ◽

Phrenic Nerve ◽

Respiratory Activity ◽

Respiratory Rhythm ◽

Related Activity ◽

Pharmacological Agents ◽

Pneumotaxic Center ◽

Trigeminal Nerves ◽

The Brain ◽

Pontomedullary Junction

We hypothesized that rhythmic respiratory-related activity could be generated in pons independent of medullary mechanisms. In decerebrate, cerebellectomized, vagotomized, paralyzed, and ventilated cats, we recorded efferent activities of the phrenic nerve and mylohyoid branch of the trigeminal nerve. Following transections of the brain stem at the pontomedullary junction, the phrenic and trigeminal nerves discharged with independent rhythms. Spontaneous trigeminal discharges eventually ceased but were reestablished after strychnine, doxapram, and/or protriptyline were administered. In some animals having no spontaneous trigeminal discharges after transection, these discharges appeared, with a rhythm different from the phrenic, following administration of these agents. In other cats having no transections between pons and medulla, these pharmacological agents induced trigeminal and phrenic discharges after kainic acid had been injected into the entire dorsal and ventral medullary respiratory nuclei. Phrenic and trigeminal discharges were linked, indicating survival of bulbospinal neurons or presence of pontospinal units. We conclude that rhythms, similar to respiratory rhythm, can occur by mechanisms in isolated pons. Such mechanisms are hypothesized to be within the pneumotaxic center and may underlie the neurogenesis of eupnea.

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Differing responses to hypercapnia and hypoxia following pneumotaxic center ablation

Respiration Physiology ◽

10.1016/0034-5687(75)90066-3 ◽

1975 ◽

Vol 23 (1) ◽

pp. 1-9 ◽

Cited By ~ 20

Author(s):

Walter M.S.T. John

Keyword(s):

Pneumotaxic Center

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Distribution of GABAergic Neurons in the Nuclei of the Pneumotaxic Center in the Early Postnatal Period in Health and Prenatal Insufficiency of the Serotoninergic System in Rats

Neuroscience and Behavioral Physiology ◽

10.1007/s11055-015-0203-8 ◽

2015 ◽

Vol 46 (1) ◽

pp. 95-99

Author(s):

L. I. Khozhai

Keyword(s):

Postnatal Period ◽

Gabaergic Neurons ◽

Early Postnatal Period ◽

Serotoninergic System ◽

Pneumotaxic Center

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Intraoperative Pontine Infarction: A Hidden Challenge

Case Reports in Anesthesiology ◽

10.1155/2012/807398 ◽

2012 ◽

Vol 2012 ◽

pp. 1-2

Author(s):

Nicholas Marcanthony ◽

Ehab Farag

Keyword(s):

Breathing Pattern ◽

Postanesthesia Care Unit ◽

The Core ◽

Neurological Intensive Care ◽

Abnormal Breathing ◽

Gag Reflex ◽

Pneumotaxic Center ◽

Clinical Changes ◽

The Brain ◽

Pontine Infarct

Apneusis, or apneustic respirations, is characterized by an abnormal breathing pattern involving gasping and the inability to fully expire. A loss of gag reflex and other cranial nerve deficits are also often accompanied with these respiratory changes. In neurological intensive care units (NICUs), these respiratory and airway changes are not uncommon and have been well documented (Lee et al. 1976). These clinical changes are often associated with pontine trauma as it is the core pneumotaxic center in the brain stem. We describe the airway management of a patient with an acute, occult pontine infarct status post craniectomy and cervical laminectomy for decompression of known Chiari malformation in the postanesthesia care unit (PACU).

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Effects of potassium depletion on control of breathing in awake rats

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1976.231.2.588 ◽

1976 ◽

Vol 231 (2) ◽

pp. 588-592 ◽

Cited By ~ 7

Author(s):

EE Nattie ◽

SM Tenney

Keyword(s):

Breathing Pattern ◽

Ventilatory Response ◽

Inhibitory Effect ◽

Catecholamine Metabolism ◽

Membrane Excitability ◽

Acid Base ◽

Pneumotaxic Center ◽

Low K ◽

Base Data ◽

K Depletion

Possible mechanisms for the variable ventilatory response to metabolic acid-base disturbances have been examined in normal and K-depleted rats. Ventilatory measurements are correlated with CSF acid-base data. The ratios VE/VO2 and 1/PaCO2 are utilized as indices of alveolar ventilation. The log of these indices correlates closely with CSF [H+] independent of [K+] except at very low CSF [H+] where the change in log 1/PaCO2 and log VE/VO2 per change in CSF [H+] is much diminished in low-K rats. This finding suggests the presence of an additional stimulus to breathing in the low-K rat opposing the inhibitory effect of low CSF [H+]. Otherwise the chemical control of ventilation appears to be normal. However, low-K rats always breath with a low-flight-Vt pattern and occasionally with abnormal rhythms. The similarity of the low K breathing pattern to that reported in awake animals with vagotomy and pneumotaxic center (PC) lesions suggests that the altered breathing pattern in depletion involves vagal and/or PC pathways. The similarity of the low-K breathing pattern to that observed with reserpine administration together with the known relationships of K and catecholamine metabolism lead to the speculation that K depletion alters breathing via an effect on central catecholamine metabolism. However, other mechanisms involving changes in membrane excitability and intracellular pH in K depletion might also be involved.

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