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Control of Ventilation
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The pre-Botzinger Complex is responsible for initiating rhythmic respiration and is considered to be the respiratory pacemaker. It consists of a small group of pacemaker cells which produce spontaneous rhythmic discharges and activate the motor neurons of the phrenic nerve. It is located on either side of the ventral medulla between the nucleus ambiguous and the lateral reticular nucleus, amongst the ventral respiratory group of neurons. There are μ-opioid, NK1 and 5HT receptors on the cells of the pre-Botzinger complex. Serotonin (5HT4) agonists reverse the inhibitory effects of opioids on respiration with inhibiting analgesia.
Organization of Central Respiratory Neurons
Published in Alan D. Miller, Armand L. Bianchi, Beverly P. Bishop, Neural Control of the Respiratory Muscles, 2019
Armand L. Bianchi, Rosario Pásaro
Results from the in vitro brainstem-spinal cord preparation from newborn rats (see Chapter 10) have shown the importance of the iVRG and rVRG in respiratory rhythmogenesis. A portion of this region, isolated in vitro, still retains respiratory-like activities of preinspira-tory neurons, even after surgical isolation or blockade of chemical synaptic transmission by using low Ca2+ or high Mg2+ bathing solutions.49,50 Smith and colleagues68 have defined in a 400μm-thick section of the medulla, a group of cells of the ventral medulla just caudal to the retrofacial nucleus, that they have called the “pre-Bötzinger complex”. These cells retain rhythmic respiratory-related discharge patterns even after isolation from adjacent medullary tissue. The pre-Bötzinger complex therefore appears to contain a population of neurons essential for the generation of the respiratory-like discharges observed in cranial and spinal nerve roots of this preparation. Examination of the anatomical connections of the neurons within a region of the VRG homologous to the pre-Bötzinger complex24,47 indicates that this area contains a high percentage of propriobulbar neurons; bulbospinal premotor neurons are concentrated in the VRG caudal to the pre-Bötzinger complex.
Role of the NTS in the Medullary Respiratory Network Producing Respiratory Movements
Published in I. Robin A. Barraco, Nucleus of the Solitary Tract, 2019
Armand L. Bianchi, Laurent Grélot
The STA method was fruitfully used to bring evidence for the existence of synaptic connectivity between the medullary respiratory neurons. Such evidence was first obtained for the augmenting expiratory neurons of the Bötzinger complex which appear at the origin of the late expiratory inhibition of the inspiratory NTS neurons.78 The early-burst inspiratory neurons, or decrementing inspiratory neurons, have also been shown to monosynaptically inhibit most of the inspiratory neurons, including those of the NTS.79,80
Obstructive sleep apnea: personalizing CPAP alternative therapies to individual physiology
Published in Expert Review of Respiratory Medicine, 2022
Brandon Nokes, Jessica Cooper, Michelle Cao
It is worth mentioning here that there are two chemoreceptive sensors with converging data on the respiratory pattern generator; the pre-Botzinger complex (preBotC) [54]. The carotid body is the principle O2 sensor in humans (the aortic body appears to be less relevant) [55]. This organ is unique in that it has the most blood flow per gram of tissue in the human body, allowing for rapid detection of subtle polymodal chemical cues by highly specialized glomus cells [56]. This arrangement facilitates changes in neural output in response to subtle changes in O2 partial pressure, pH, glucose, etc. Of note, there appear to be two distinct populations of glomus cells: 1) chemosensory – dopamine beta hydroxylase positive, express nicotinic receptors, elaborate norepinephrine in response to hypoxia, and are inhibited by dopamine, and 2) sympatho-excitatory – tyrosine hydroxylase positive, express purinergic receptors (P2X3), elaborate adenosine triphosphate (ATP) in response to hypoxia, and can be stimulated with angiotensin II [56,57]. These two glomus cell populations drive the ventilatory and sympathetic responses to hypoxia, respectively. These subtleties are worth considering, because medications such as anti-dopaminergic agents and anti-purinergic agents (such as Ticagrelor) can exert effects on ventilatory control stability through their actions on the carotid body [58,59].
Correlations of plasma oxytocin with clinical and hormonal parameters in panic disorder
Published in Nordic Journal of Psychiatry, 2023
Vasilios G. Masdrakis, Charalambos Papageorgiou, Manolis Markianos
However, a potential explanation for our findings may stem from the type of action that OXT exerts on the respiratory functions. The hypothalamus exerts control on the autonomic functions, since paraventricular OXT and vasopressin neurons project to brainstem nuclei involved in respiratory rhythm generation and modulation, including the pre-Botzinger complex, the ventral respiratory column and the phrenic nuclei and the nuclei of the tractus solitarius (NTS) [31]. Data from animal (cats) studies, suggest that vasopressin and OXT exert excitatory effects on the respiratory and respiration-related neurons in the nuclei of the NTS – an integral medullary region which is essential for respiratory and cardiac functions [32]. In humans with obstructive sleep apnea, OXT administered intranasally significantly increased the respiratory rate not only during obstructive, but also during non-obstructive periods as well [33]. However, these excitatory effects on the respiratory system may be counterproductive in PD patients. The reason for this comes from a wealth of previous data suggesting that PD patients demonstrate a pathological sensitivity to interoceptive or exteroceptive cues stimulating the respiratory centers, including cues designating asphyxia (e.g. [34–38]). Consequently, although higher levels of endogenous OXT may be correlated with less ‘general’ anxiety – in line with results from other human and animal populations [7–12] –, yet its effect on ‘specific’ panic psychopathology may not be evident due to the excitatory effects that OXT exerts on respiration. Noteworthy, this distinction between ‘anxiety’ and ‘panic’ as two distinct clinical phenomena, moreover with different biological underpinnings, has been stressed by Klein’s ‘suffocation alarm theory’ [34]. Moreover, this theory suggests that panic psychopathology is not associated with activation of the HPA-axis.
Prevention of sudden unexpected death in epilepsy: current status and future perspectives
Published in Expert Review of Neurotherapeutics, 2020
Max Christian Pensel, Robert Daniel Nass, Erik Taubøll, Dag Aurlien, Rainer Surges
Seizure-related respiratory disturbances with transient hypoxemia and hypercapnia occur in 33–43% of focal seizures [40–42], mostly due to central or obstructive apnea. Ictal central apnea (ICA) occurs in one-third of seizures with focal onset and 43% of patients, especially when arising from sleep and from temporal lobes; the recurrence risk in a given patient amounts to 75%. Postconvulsive central apnea (PCCA) occurs in one-fifth of TCS with focal or generalized onset and 22% of patients, especially in women; the recurrence risk in a given patient amounts to 53% [43]. PCCA is considered as a possible biomarker for SUDEP, as in a recent case series it was reported in association with asystole in two cases and in one person who later died of SUDEP [44,45]. In this context, CO2-dependent arousal mechanisms and serotonin signaling are also discussed to contribute to the fatal cascade [46]. Increased levels of serotonin are thought to inhibit seizures and some AEDs may at least partially exert their clinical effects via enhancing extracellular serotonin [47]. Importantly, serotoninergic neurons in the brain stem have an impact on many different functions and networks in the brain, among others on arousal and control of breathing. Data from animal models suggest that postictal deficits in serotoninergic signaling could lead to or aggravate hypoventilation and impair arousal reaction to postictally elevated CO2 levels [47]. For instance, in DBA/1 and DBA/2 mouse models with audiogenic reflex-seizures and subsequent respiratory arrest, administration of serotonin reuptake inhibitors (SRIs) prevented respiratory arrest [48] and 5HT2 c-receptor knockout-mice often die after seizure-related apnea, indicating the relevance of serotoninergic neurons in the development of central apneas [49]. In humans, postmortem analysis of the ventrolateral medulla, especially of the pre-Bötzinger complex and the medullary raphe nuclei showed greater reductions of neuron populations and neuromodulatory neuropeptidergic and mono-aminergic systems involving serotonin and galanin in SUDEP patients as compared to controls [50]. Furthermore, blood serotonin levels were found to be elevated after seizures without ICA or PCCA, but not after seizures with ICA or PCCA [51]. Likewise, the duration of PGES was inversely correlated with interictal serotonin blood levels, prompting the hypothesis that blood serotonin levels play a role in shaping seizure features or may partly reflect serotonin levels in the CNS [52]. The hypothesis that serotonin levels have an impact on seizure features is further supported by the observation that patients taking SRIs display less frequently ICA, and patients on chronic treatment with benzodiazepines have shorter ICA and PGES durations [53,54].