Relevant bibliographies by topics / Laryngeal chemoreflex

Academic literature on the topic 'Laryngeal chemoreflex'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Laryngeal chemoreflex"

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Goding, George S., and Kerri Johnson Pernell. "Effect of a Second Laryngeal Stimulation during Recovery from the Laryngeal Chemoreflex." Otolaryngology–Head and Neck Surgery 114, no. 1 (January 1996): 84–90. http://dx.doi.org/10.1016/s0194-59989670288-7.

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The laryngeal chemoreflex is a potential mechanism for sudden infant death. In experimental protocols in which a full recovery is allowed between stimuli, no laryngeal chemoreflex responses result in a fatal outcome. In the clinical situation there are no controls to prevent repeated laryngeal stimulation before a full recovery. The effect of a laryngeal stimulus applied during or soon after a laryngeal chemoreflex-induced apnea was investigated. Eighteen piglets were divided into groups aged 10 to 12 days, 17 to 21 days, and 32 to 36 days. Laryngeal stimulation was performed under normoxic conditions with water applied to the mucosa. Baseline respiratory and cardiovascular response data were measured. After recovery an initial stimulation was applied, followed by a second stimulation during the apnea or 5, 30, 60, or 120 seconds after restoration of breathing. No profound apneas occurred with baseline laryngeal stimulation. In piglets aged 32 to 36 and 17 to 21 days, a second laryngeal stimulus resulted in a shortened apnea duration. The response varied in piglets aged 10 to 12 days with profound apneas observed In 2 of 6 subjects and 4 of 30 trials. Piglets aged 17 to 36 days are less susceptible to the laryngeal chemoreflex during the immediate recovery period. In piglets aged 10 to 12 days, the laryngeal chemoreflex response may be more severe after a second Stimulus.
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Chan, Kenneth, Linda K. Kullama, Linda Day, Anthony Ogundipe, and Michael G. Ross. "Ovine Fetal Laryngeal Chemoreflex Thresholds and Respiratory Effects." Otolaryngology–Head and Neck Surgery 116, no. 1 (January 1997): 91–96. http://dx.doi.org/10.1016/s0194-59989770356-5.

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In newborn infants, laryngeal contact with solutions of low chloride concentration or pH evokes swallowing, laryngeal adduction, and respiratory inhibition (laryngeal chemoreflex). To determine whether the laryngeal chemoreflex is present during fetal life and its effect on fetal respiratory activity, eight time-bred ewes (128 ± 2 days) were prepared with fetal electrocortical diaphragm and esophageal electrodes and a nasopharyngeal catheter. After a 60-minute control period, increasing volumes (0.1 to 1.0 ml/kg) of 0.15 mol/L NaCl or distilled water (0.05 to 1.0 ml/kg) and decreasing concentrations of NaCl (0.15 to 0.02 mol/L) at a fixed volume (0.3 ml/kg) were sequentially administered through the nasopharyngeal catheter (38° C). The minimum water volume that stimulated swallowing was significantly less than the minimum 0.15 mol/L NaCl volume (0.10 ± 0.02 vs. 0.70 ± 0.05 ml/kg). The maximum NaCl concentration that stimulated swallowing was 0.04 ± 0.01 mol/L. During the control period, respiratory activity averaged 14.6 ± 0.7 breaths/minute and did not change during absent swallow responses or isotonic saline-induced swallows. However, respiratory activity significantly decreased during water (4.7 ± 0.6 breaths/minute) and hypotonic saline-induced swallow responses (3.7 ± 0.7 breaths/minute). Fetal electrocortical activity did not change during absent or stimulated swallows. We conclude that laryngeal water or hypotonic saline solution may stimulate fetal swallowing and suppress fetal respiratory activity, similar to the newborn laryngeal chemoreflex. We speculate that an exaggeration of the laryngeal chemoreflex apnea response in the newborn may predispose to sudden infant death syndrome.
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Goding, George S. "Correlation of Laryngeal Chemoreflex Severity With Laryngeal Muscle Response." Laryngoscope 108, no. 6 (June 1998): 863–72. http://dx.doi.org/10.1097/00005537-199806000-00015.

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Park, Han-Q., Won-Pyo Hong, Kwang-Moon Kim, Myung-Sang Kim, Young-Ho Kim, and Dong-Young Kim. "Age Dependence of Laryngeal Chemoreflex in Puppies." Annals of Otology, Rhinology & Laryngology 110, no. 10 (October 2001): 956–63. http://dx.doi.org/10.1177/000348940111001012.

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Previously collected data have indicated that the laryngeal chemoreflex (lcr) response is exaggerated during a critical period of postnatal development in several experimental animals. These animals had fewer anatomic and physiological similarities to humans than do puppies. This investigation of the lcr in 14 anesthetized puppies was undertaken to determine age-related differences in the response to stimulation of the supraglottic laryngeal mucosa by saline solution, distilled water, cow's milk, and acid at pH 1.0. The dogs were divided into 3 age groups: group 1 consisted of 4 dogs that were 2 weeks old, and in groups 2 and 3 there were 5 puppies each, of 4 and 6 weeks of age, respectively. The lcr response (laryngospasm, apnea, respiratory depression, and bradycardia) was found in the puppies only after stimulation of the laryngeal mucosa with acid at pH 1.0, and it was more easily achieved in the 4- and 6-week age groups than in the 2-week group. These findings suggest that the lcr is an age-dependent response that appears in dogs only after 2 weeks of age. The important implication of this finding is that postnatal neural maturation may influence the laryngeal reflex in humans to some extent.
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Woodson, Gayle E., and George Brauel. "Arterial chemoreceptor influences on the laryngeal chemoreflex." Otolaryngology–Head and Neck Surgery 107, no. 6_part_1 (December 1992): 775–82. http://dx.doi.org/10.1177/019459988910700612.1.

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Prolonged apnea and cardiovascular changes have been elicited in infant animals by the application of water to the laryngeal mucosa. Previous reports have produced conflicting evidence in regard to the possible role of arterial chemoreceptors in modulating this reflex. The present study was designed to determine the effect of carotid body stimulation or suppression on the duration of apnea and severity of cardiovascular changes in response to water in the larynx of piglets. The role of swallowing in terminating the apnea was also Investigated. Hypoxia and isoproterenol, both carotid body stimuli, caused decreased apnea duration. Hyperoxia was associated with prolonged apnea duration; however, dopamine, which inhibits carotid body chemoreceptors, produced no significant change. Hypotension and bradycardia were only observed after prolonged apnea or chemoreceptor stimulation, supporting the concept that the cardiovascular component of the laryngeal chemoreflex is a result of changes in blood gas concentration rather than a direct response to laryngeal chemostimulatlon. The Interval between water application and Initiation of swallowing was not significantly affected by hypoxia or carotid body stimulation and swallowing did not always occur before resumption of breathing.
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Wang, Deqiang, Timothy M. McCulloch, Nancy M. Bauman, Debra M. Jaffe, Richard J. H. Smith, Michael P. Porter, and Anthony D. Sandler. "Role of Substance P in the Laryngeal Chemoreflex." Annals of Otology, Rhinology & Laryngology 107, no. 7 (July 1998): 575–80. http://dx.doi.org/10.1177/000348949810700706.

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The laryngeal chemoreflex (LCR) is a potentially life-threatening reflex that is elicited in immature animals by the topical application of water to the laryngeal mucosa. The reflex response is characterized by immediate apnea and laryngeal adduction and delayed cardiovascular instability. The cardiorespiratory changes of the LCR may be life-threatening, particularly in very immature animals such as piglets under 2 weeks of age. The afferent and efferent limbs of the LCR are mediated through the vagus nerve, but the neuromediators responsible for the reflex changes have not yet been clearly elucidated. Previous agonist and antagonist studies in immature dogs demonstrated that substance P, a sensory tachykinin, mediates the life-threatening esophagolaryngeal adductor reflex elicited by distal esophageal sensory nerve stimulation. This study was conducted to determine if substance P also plays a role in mediating the LCR. The LCR response was compared before and after treatment with intravenous substance P antagonist (Pfizer CP-96,345–1) in eight piglets (mean 27.7 days of age). The laryngeal and cardiovascular responses of the animals following intravenous administration of the tachykinins substance P, neurokinin a, and neurokinin B were also assessed. Pretreatment with substance P antagonist did not alter the LCR's duration of apnea (p > .10), laryngeal adductor response, or early change in mean arterial pressure (p > .10), although the early maximal heart rate response was significantly altered (p < .01). Intravenous substance P, neurokinin a, and neurokinin B did not reproduce the laryngeal respiratory response of the LCR. We conclude that substance P, neurokinin a, and neurokinin B are not key neurotransmitters of the LCR.
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Pathak, Shivani, Laurie Slovarp, Matthew S. Clary, and Marie E. Jetté. "Laryngeal Chemoreflex in Health and Disease: A Review." Chemical Senses 45, no. 9 (October 14, 2020): 823–31. http://dx.doi.org/10.1093/chemse/bjaa069.

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Abstract The larynx plays a key role in airway protection via the laryngeal chemoreflex (LCR). This involuntary reflex can be evoked when hazardous substances activate mucosal receptors, which send signals to be processed within the brainstem. Although the LCR is meant to be protective, the reflex can become hyperstimulated, even to benign stimuli, which can result in pathological disorders, such as chronic cough and inducible laryngeal obstruction. In this review, we will outline the mechanism of the LCR and its associated pathological disorders.
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Wei, Wan, Xiuping Gao, Lei Zhao, Jianguo Zhuang, Yang Jiao, and Fadi Xu. "Liquiritin apioside attenuates laryngeal chemoreflex but not mechanoreflex in rat pups." American Journal of Physiology-Lung Cellular and Molecular Physiology 318, no. 1 (January 1, 2020): L89—L97. http://dx.doi.org/10.1152/ajplung.00306.2019.

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Liquiritin apioside (LA), a main flavonoid component of licorice, reportedly suppresses cough responses to inhalation of aerosolized capsaicin [CAP; a stimulant to transient receptor potential vanilloid 1 (TRPV1)] in conscious guinea pigs via acting on peripheral nerves. However, the evidence of LA having a direct effect on airway sensory fibers is lacking. Considering the important role laryngeal chemoreceptors and mechanoreceptors play in triggering apnea and cough, we studied whether LA suppressed the apneic responses to stimulation of these receptors via directly acting on the superior laryngeal nerve (SLN). Intralaryngeal delivery of chemical [CAP, HCl, and distilled water (DW)] and mechanical [an air-pulse (AP)] stimulations was applied in anesthetized rat pups to evoke the apnea. These stimuli were repeated after intralaryngeal LA treatment or peri-SLN LA treatment to determine the direct effect of LA on the SLN. Our results showed that all stimuli triggered an immediate apnea. Intralaryngeal LA treatment significantly attenuated the apneic response to chemical but not mechanical stimulations. The same attenuation was observed after peri-SLN LA treatment. Owing that TRPV1 receptors of laryngeal C fibers are responsible for the CAP-triggered apneas, the LA impact on the activity of laryngeal C neurons retrogradely traced by DiI was subsequently studied using a patch-clamp approach. LA pretreatment significantly altered the electrophysiological kinetics of CAP-induced currents in laryngeal C neurons by reducing their amplitudes, increasing the rise times, and prolonging the decay times. In conclusion, our results, for the first time, reveal that LA suppresses the laryngeal chemoreceptor-mediated apnea by directly acting on the SLN (TRPV1 receptors of laryngeal C fibers).
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Downs, Daniel H., Kerri Johnson, and George S. Goding. "The effect of antitastamines on the laryngeal chemoreflex." Laryngoscope 105, no. 8 (August 1995): 857–61. http://dx.doi.org/10.1288/00005537-199508000-00017.

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Boyer, H. C., D. H. Downs, G. S. Goding, and K. J. Pernell. "Effect of Topical Diphenhydramine on the Laryngeal Chemoreflex." Archives of Otolaryngology - Head and Neck Surgery 122, no. 10 (October 1, 1996): 1112–16. http://dx.doi.org/10.1001/archotol.1996.01890220078013.

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Dissertations / Theses on the topic "Laryngeal chemoreflex"

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Donnelly, William T. "Serotonin Signaling in the Nucleus Tractus Solitarius Modulates the Laryngeal Chemoreflex| Implications for Sudden Infant Death Syndrome." Thesis, Dartmouth College, 2016. http://pqdtopen.proquest.com/#viewpdf?dispub=10145494.

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Sudden infant death syndrome (SIDS) occurs when a sleeping infant experiences a challenge to cardiorespiratory homeostasis which it fails to overcome. Analyses of brain tissue from SIDS cases from around the world consistently show abnormalities in the brainstem serotonin systems. These include increased numbers of neurons that test positive for serotonergic markers, but have an immature phenotype, reduced brain tissue serotonin concentrations and decreased serotonin receptor binding in projection sites important to cardiorespiratory homeostasis, including the nucleus of the solitary tract (NTS). The NTS is of particular interest in the pathophysiology of SIDS because it is the integration center for afferent projections involved in eliciting several apnea-inducing reflexes long suspected of contributing to SIDS. The laryngeal chemoreflex (LCR), an airway protective reflex which is initiated when water, acidic solutions, or low [Cl-] solutions activate chemoreceptors in the larynx, is one such reflex. In infants, inhibitory reflex responses to hypoxia (apnea, bradycardia, decreased metabolic activity) that are adaptive for a fetal environment that precludes the possibility of the fetus acquiring more oxygen by increasing breathing, persist for some time into the postnatal period. Therefore, hypoxia resulting from apnea caused by the LCR can result in a cataclysmic downward spiral of apnea, followed by increasing hypoxic inhibition of respiration, which ultimately leads to SIDS. We hypothesized that increasing serotonin signaling in the brainstems of rat pups would shorten the apnea and respiratory disruption caused by eliciting the LCR. We have shown that both intracisternal injections of serotonin, and microinjections of serotonin into the caudal NTS, dramatically shorten the LCR. This effect is also seen after microinjection into the NTS of the 5-HT3 specific agonist CPG. Chemical stimulation by microinjection of AMPA of neurons in the raphe obscurus, some of which send serotonergic projections to the NTS, also shortens the LCR, but this effect is blocked by prior injection of a 5-HT3 antagonist in the NTS. Our work suggests that serotonergic projections to the NTS from the caudal raphe may play an important role in limiting the duration of apnea following inhibitory reflexes like the LCR and in the subsequent restoration of eupnea.

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Book chapters on the topic "Laryngeal chemoreflex"

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Xia, Luxi, Tracey Damon, J. C. Leiter, and Donald Bartlett. "Elevated Body Temperature Exaggerates Laryngeal Chemoreflex Apnea in Decerebrate Piglets." In Integration in Respiratory Control, 249–54. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-73693-8_44.

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Conference papers on the topic "Laryngeal chemoreflex"

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Dragomir, A., Y. Akay, and M. Akay. "Investigating the Complexity of Respiratory Patterns during the Laryngeal Chemoreflex." In 6th International Special Topic Conference on Information Technology Applications in Biomedicine, 2007. IEEE, 2007. http://dx.doi.org/10.1109/itab.2007.4407420.

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St-Hilaire, M., C. Duvareille, O. Avoine, AM Carreau, and JP Praud. "Effects of Passive Smoking on Laryngeal Chemoreflexes in Newborn Lambs." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1752.

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Samson, Nathalie, Nadia Boudaa, Vincent Carriere, and Jean-Paul Praud. "Nasal Continuous Positive Airway Pressure Improves The Cardiorespiratory Components Of Laryngeal Chemoreflexes Contrarily To Caffeine Treatment In Preterm Lambs." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a6667.

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